by @ Archive - Articles

Mon Aug 29 16:46:25 PDT 2011

LongeCity continues to support small-scale, high-impact life extension research with community crowdfunding.
(For a review of previous projects see here)

Projects should:- aim to make a scientific contribution to the extension of the human lifespan
- be applied research or basic research with some potential for applied development
- present short updates for LongeCity Members with interim data, photos from the facility etc at agreed intervals
- be led or overseen by a person with a postgraduate qualification in the relevant field or by a person with demonstrable equivalent experience
- have a flexible project structure that can be adjusted according to the amount of money raised
- be small in scale - one or two key workers
- be short in duration - approx 6 months maximum
- not be confidential. LongeCity will expect open and public presentation and discussion of research results. However, confidentiality will be accepted where a manuscript or patent is in preparation.

In 2013, we are not just matching, but trebling donationsLongeCity will launch a call for donations. Every donation received will be trebled. Projects can have a total budget of $3.000- $21.000. (Hence needing to raise only $1.000-$7.000)

Interested applicants should send
- a project outline of no more than 1000 words written in lay language (can be supported by up to 10 literature references)
- a curriculum vitae of the project leader
to research@longecity.org

by @ Articles - Articles

is led by life-extension trailblazer Kelsey Moody. It is interesting that he turns the attention of his new venture Ichor Therapeutics to the potential health effects of 'buckyballs' - a topic that has received significant attention on LongeCity ever since it was claimed in a scientific report that rats fed on olive oil infused with these structures experience dramatically increased maximal lifespans. (Review here). True to it mission, LongeCity hosts the leading international discussion forum on this topic. Previously, the LongeCity community has come together to fund further grassroots research on C60 in mice and these studies are on-going.

Meanwhile though, in keeping with the pioneer spirit often found on the LongeCity forums, reports have come in from people trialing C60 in olive oil on themselves. As Kelsey points out, the long-term safety of this has yet to be established, and this project is particularly interested in whether C60 in olive oil has any cancer-inducing properties. Conversely, it may be the case that the compound has a tumor–suppressing function. To investigate this, the team plans to infuse a total of 25 mice with C60-olive oil of various strengths or with an inert ‘control’ solution, graft a human cancer cell line to the mice and study the results. (Full research proposal here)

If the fundraiser succeeds it will further support the revolutionary notion of stakeholder-oriented, grass-roots science which complements, challenges and enriches academic research at those junctures that the community actually cares about. Moreover and perhaps even more importantly the fundraiser will help to built capacity and community interface at a dedicated life-extension research facility. Already, Ichor has housed an intern on a LongeCity stipend (Report here- Members only). Ultimately, we hope to create a network of such community-friendly labs around the globe, to provide aspiring young scientistswith training and networking and all members with easily accessible sources of expert advice.

LongeCity has facilitated 'crowdfunding' well before many other platforms in use today. This year, we have decided to try to tap into the potential of these external sites, but to add something to the process: This project is the first one to run on an external fundraising page that has received an official ‘stamp of endorsement’ from LongeCity.The team has mooted the project at LongeCity, submitted for formal peer review and informal members comments and the board looked into the ability of the team to use the donated money responsibly and to deliver success (Internal link here). In the end, the project received a high rating of 3 stars and LongeCity decided to match each dollar donation from our general funds. And, awesomely, a generous Member immediately stepped forward to match them as well!

by Owen Alexander @ Alt Protein

Tue Jan 23 13:08:30 PST 2018

If you’re like most people, you’ve probably seen a plethora of smoothie recipes scattered all over Pinterest or Facebook. Most recipes include at least a cup of yogurt that’s thrown into your blender, and then you’re supposed to add a variety of vegetables and/or fruits into the blender. Once you’ve got everything inside of your ... Read moreThe Best Smoothie Recipes Without Yogurt

by @ Action

However, given the recent successes and highly emotional nature of life extension research, Aubrey de Grey is not the first, nor will he be the last, to promote a hopelessly insufficient but ably camouflaged pipe-dream to the hopeful many. With this in mind, we hope our list provides a general line of demarcation between increasingly sophisticated life extension pretense, and real science and engineering, so that we can focus honestly on the significant challenges before us.

May be when the mission, vision and goals of a company, or in this case a research foundation and public charity in financial distress, sound too good to be true the alarm bell should be ringing.

After 8 years since its foundation (2009) is there any available tested application/therapy coming out from SENS line of research?

People who have fibromyalgia are also more likely to suffer from sleep disorders, chronic fatigue, depression, headaches, IBS, lupus, arthritis and post-traumatic stress disorder. According to Katherine Zerensky, nutritionist at the Mayo Clinic, probiot

by @ LongeCityNews

Sun Feb 11 01:51:59 PST 2018

Fight Aging! provides a weekly digest of news and commentary for thousands of subscribers interested in the latest longevity science: progress towards the medical control of aging in order to prevent age-related frailty, suffering, and disease, as well as improvements in the present understanding of what works and what doesn't work when it comes to extending healthy life. Expect to see summaries of recent advances in medical research, news from the scientific community, advocacy and fundraising initiatives to help speed work on the repair and reversal of aging, links to online resources, and much more.

This content is published under the Creative Commons Attribution 4.0 International License. You are encouraged to republish and rewrite it in any way you see fit, the only requirements being that you provide attribution and a link to Fight Aging!

Aging and cancer are conceptually similar in many ways, and by this I mean that they are both collections of processes that are fundamental to the way in which the biology of complex organisms works. They are not states that can be cured or eliminated through medicine as we presently understand it, but the aspiration is instead to bring these undesirable outcomes under control - to continually cut back the offshoots, to suppress the causes, and nip in the bud the results of those causes in their earliest stages. To actually cure either aging or cancer, to remove it from the human condition, would require a radical reworking of our cellular biochemistry, to the point at which it would cease to be biology in any meaningful sense and become a hybrid form of molecular nanotechnology. That sort of project lies far distant in the future. Today's concerns are entirely directed towards the control of aging and cancer, something that can be achieved through forms of medicine we can recognize and understand.

Regardless, we all use words carelessly. We search for cures for cancer. We call cancer a disease, though in reality this probably stretches that term as well. We choose not to call aging a disease, though not for any particularly rational reason. Having watched the progression of rejuvenation research since just after the turn of the century, it is both gratifying and interesting to see the changing tone in media coverage of the science, the message of the patient advocates, and the aspirations of those involved. Ten years ago, mockery was commonplace. Now journalists are taking it a lot more seriously; it is hard to do otherwise, given the earnest levels of funding and many scientific papers devoted to - to pick one example - the clearance of senescent cells, an actual, honest-to-goodness rejuvenation therapy now under development in various startup companies.

Nonetheless, journalistic habits of balance remain. Faced with a movement whose members want to prevent the majority of all death and suffering in the world by bringing an end to aging, and are mustering increasingly credible science to that cause, the authors of the old media still feel obliged to put in a word for the other side. After all, what about the view that everyone should just suffer and die? Why shouldn't that be presented with equal weight? After a certain point, balance becomes a caricature of itself - isn't this the sort of thing that would be put forth as satire in an earlier era? And yet here we are, death for everyone as the balance viewpoint in articles on the future rejuvenation biotechnology.

The Ambitious Quest to Cure Aging Like a Disease

The list of diseases humankind has managed to defeat is impressive. But throughout history, humans have suffered from a condition that they have never been able to escape - ageing. As we get older, our cells stop working as well and can break down, leading to conditions like cancer, heart disease, arthritis and Alzheimer's disease. Together, ageing-related diseases are responsible for 100,000 deaths per day and billions are spent around the world trying to slow their steady march on our bodies.

Some researchers, however, believe we may be thinking about these conditions in the wrong way. They say we should start treating ageing itself as a disease - one that can be prevented and treated. Their hopes are founded on recent discoveries that suggest biological ageing may be entirely preventable and treatable. From a biological perspective, the body ages at different rates according to genetic and environmental factors. Tiny errors build up in our DNA and our cells begin developing faults that can accumulate into tissue damage. The extent of these changes over time can mean the difference between a healthy old age or one spent housebound and afflicted by chronic diseases.

The scientists who hope to do this sit on the fringes of the mainstream medical landscape. But there are now a number of research centres around the world that have made identifying ways of preventing biological ageing a priority. Studies in animals have shown that it is indeed possible to dramatically extend the lifespan of certain species, giving hope that it could also be possible in humans. One of the leading figures in human longevity research, Aubrey de Grey, is the chief science officer at the Strategies for Engineered Negligible Senescence (SENS) Research Foundation, a California-based regenerative medicine research foundation focused on extending the healthy human lifespan. Their goal is to develop a suite of therapies for middle-aged and older people that will leave them physically and mentally equivalent to someone under the age of 30. They want "to fix the things we don't like about the changes that happen between the age of 30 and the age of 70". There are seven biological factors de Grey argues are predominantly responsible for cellular damage that accompanies ageing and underlies ageing-related diseases.

De Grey doesn't think that it will be possible stop ageing altogether with these types of approaches, but they may give patients an extra 30 years or so of life. He envisages a future where "rejuvenation technologies" can be administered to old people in order to revert their cells to what they were like when they were in their youth, buying them extra time. The idea is that someone who is treated at the age of 60 will be biologically reverted to 30. But because the therapies are not permanent fixes, their cells will end up becoming 60 years old again in another 30 years time. By then de Grey hopes the therapies could be reapplied as "version 2.0" to revert the same individuals once again to become younger in their cells. As a result, that person's cells wouldn't become 60 again until they're about 150 years old.

And he is not alone in believing ageing-related diseases can be solved. George Church, a geneticist at Harvard Medical School, told us that while some of his colleagues argue many age-related diseases are so complex that they simply can't be treated, he finds such thinking to be incorrect. "If you can control both the environment and the genetics, you can get people that live youthful healthy lives for exceptionally much longer than others. In industrialised nations, most of the diseases are due to age-related diseases and I think those too can be handled."

But regardless of how it is achieved, extending human lifespans by decades or even hundreds of years will present us with some difficult social realities. There could be major societal impacts if we all start living longer. There are some that fear greater longevity could lead to swelling populations and raise doubts that our planet could support such numbers. Aubrey de Grey has little time for such questions and believes that other technologies - such as artificial meat, desalination, solar energy and other renewables - will increase the carrying capacity of the planet, allowing more people to live longer lives. But this rationale suffers from a dependence on uncertain techno-fixes that may not alleviate suffering in an equally distributed manner. Yet, if concerns like these had paralysed the early pioneers of vaccination and antibiotics, it is unlikely many of us today could expect to live much beyond the age of 40-years-old. Advances in medicine over the last two centuries have taught us that we have the power to defeat the diseases that afflict us. Perhaps if we apply ourselves, then we can beat ageing too.

The brain is locked away from the biochemistry of the rest of the body behind the blood-brain barrier, the sheath of specialized cells surrounding blood vessels in the brain that prevents most unwanted molecular traffic to and from neural tissues. The brain is biochemically quite different from the rest of the body, and many of the commonplace molecules found elsewhere can be harmful to brain tissue or degrade neural function. Pericytes are one of the supporting cell types involved in the structure of the blood-brain barrier, and in the research noted here, pericyte dysfunction is linked to other known aspects of biochemical disarray in the vascular system that take place with aging. These include: the leakage of fibrinogen into the brain and its damaging effects on nerves; the progressive failure of blood-brain barrier integrity, allowing other forms of leakage; the buildup of protein aggregates that harm neurons; and the general vascular dysfunction that impacts the delivery of nutrients to the energy-hungry brain.

What can be done about this? The research here identifies the functional failure of pericytes as the earliest cause in the stack of consequences that the authors examined, but they look at managing fibrinogen as the first option for therapies. This is a sadly common sort of approach, meaning to work on the manipulation of consequences rather than addressing lower causes. To my eyes, the better way forward would be to dig deeper into the dysfunction of the cells of the blood-brain barrier, to ask why they are declining. There is a rich literature of investigation regarding blood vessel dysfunction, one that is starting to touch on the contributions of the root causes of aging, such as cellular senescence. More could certainly be done in that direction, rather than immediately preparing the ground for attempts at clinical translation of what has been learned so far.

Half of all dementias, including Alzheimer's, start with damaged 'gatekeeper cells'

Nearly 50 percent of all dementias, including Alzheimer's, begins with the breakdown of the smallest blood vessels in the brain and their protective "gatekeeper cells," according to a new study. That catastrophe causes a communications failure called small vessel disease. Many people with that disease also have white matter disease, the wearing away of fatty myelin that allows neurons to transfer messages within the brain network. In an animal model, researchers found that brain deterioration associated with dementia may start as early 40 in humans.

For more than 25 years, scientists have known that white matter disease impedes a person's ability to learn or remember new things, slows thinking and causes people to fall more often due to balance issues. They identified a link between crippled small blood vessels in the brain and white matter disease but didn't know what started that process until now. "Many scientists have focused their Alzheimer's disease research on the buildup of toxic amyloid and tau proteins in the brain, but this study and others from my lab show that the problem starts earlier - with leaky blood vessels in the brain. The collapse of pericytes - gatekeeper cells that surround the brain's smallest blood vessels - reduces myelin and white matter structure in the brain. Vascular dysfunctions, including blood flow reduction and blood-brain barrier breakdown, kick off white matter disease."

The study explains that pericytes play a critical role in white matter health and disease via fibrinogen, a protein that circulates in blood. Fibrinogen develops blood clots so wounds can heal. When gatekeeper cells are compromised, an unhealthy amount of fibrinogen slinks into the brain and causes white matter and brain structures, including axons (nerve fibers) and oligodendrocytes (cells that produce myelin), to die. The researchers are the first to show that fibrinogen is a key player in non-immune white matter degeneration. The protein enters the brain through a leaky blood-brain barrier. The study found about 50 percent fewer gatekeeper cells and three times more fibrinogen proteins in watershed white matter areas in postmortem Alzheimer's brains of humans compared to healthy brains.

To confirm that fibrinogen proteins are toxic to the brain, researchers used an enzyme known to reduce fibrinogen in the blood and brain of mice. White matter volume in mice returned to 90 percent of their normal state, and white matter connections were back to 80 percent productivity. "Our study provides proof that targeting fibrinogen and limiting these protein deposits in the brain can reverse or slow white matter disease. It provides a target for treatment, but more research is needed. We must figure out the right approach. Perhaps focusing on strengthening the blood-brain barrier integrity may be an answer because you can't eliminate fibrinogen from blood in humans. This protein is necessary in the blood. It just happens to be toxic to the brain."

Diffuse white-matter disease associated with small-vessel disease and dementia is prevalent in the elderly. The biological mechanisms, however, remain elusive. Using pericyte-deficient mice, magnetic resonance imaging, viral-based tract-tracing, and behavior and tissue analysis, we found that pericyte degeneration disrupted white-matter microcirculation, resulting in an accumulation of toxic blood-derived fibrin(ogen) deposits and blood-flow reductions, which triggered a loss of myelin, axons, and oligodendrocytes. This disrupted brain circuits, leading to white-matter functional deficits before neuronal loss occurs.

Fibrinogen and fibrin fibrils initiated autophagy-dependent cell death in oligodendrocyte and pericyte cultures, whereas pharmacological and genetic manipulations of systemic fibrinogen levels in pericyte-deficient, but not control mice, influenced the degree of white-matter fibrin(ogen) deposition, pericyte degeneration, vascular pathology and white-matter changes. Thus, our data indicate that pericytes control white-matter structure and function, which has implications for the pathogenesis and treatment of human white-matter disease associated with small-vessel disease.

In the open access paper noted here, researchers use modeling to suggest that age-related decline of the thymus, and thus of the immune system, is more important than mutation as a determinant of cancer risk. Cancer is at root caused by mutational damage to DNA. While DNA repair and replication mechanisms are highly efficient, mutations nonetheless occur - and must occur at some rate in order for evolution to take place. It is a numbers game, in that the more time, the more cells, and the more cell activity, the greater the odds that a cancerous mutation will occur. Mutation rates are also affected by external factors such as radiation, toxic molecules in the cellular environment, and other forms of stress put upon cells. But this is just the primary cause, the trigger enables a cell to replicate without restraint.

After a mutation occurs, there are several classes of process that work to shut down or destroy potentially cancerous cells. We suffer countless potential cancers in our lives, but near all are suppressed before they start. The first line of defense is internal to cells: mechanisms such as those related to p53 that can respond to cancerous mutations and aberrant behavior by inducing immediate programmed cell death or inducing the state of cellular senescence. The latter shuts down replication, sets the cell on the path to self-destruction via apoptosis, and further issues signaling that calls in the immune system to destroy the errant cell. The immune system is the second, and perhaps more important line of defense. Immune cells of various types aggressively seek out and destroy cells that show signs of cancer or other undesirable behavior.

Unfortunately, the immune system declines in effectiveness with age. One of the reasons for this decline is a slowing of the rate at which new T cells are created. This is in part a question of the loss of stem cell activity that occurs throughout the body, reducing the generation of new cells of all sorts. Perhaps more important in the case of T cells is the age-related atrophy of the thymus, however. This organ is where T cells mature before taking up their assigned roles in the body. It is highly active in childhood, but the active tissue begins to be replaced by fat at the onset of maturity, a process called involution. This continues over a life span and into old age, and the pace at which new T cells mature falls along with it.

A slow rate of T cell replacement causes the existing specialized and active T cell populations to become ever more worn and ragged, lacking reinforcements that can respond effectively to new challenges. This affects most of the aspects of immune function, from the response to invading pathogens to the ability to catch and destroy cancerous cells before they start in earnest the process of generating a tumor. For this reason there is considerable interest in the research community in finding ways to rejuvenate the thymus, to restore the active tissue that acts as a nursery for T cell maturation. If successful, this should go some way towards regaining the lost capacity of the immune system.

Thymic involution and rising disease incidence with age

T cells develop from hematopoietic stem cells as part of the lymphoid lineage and have the ability to detect foreign antigens and neoantigens arising from cancer cells. In the thymus, lymphoid progenitors commit to a specific T cell receptor and undergo selection events that screen against self-reactivity. Cells that pass these selection gates then leave the thymus, clonally expanding to form the patrolling naive T cell pool.

The vast majority of vertebrates experience thymic involution (or atrophy) in which thymic epithelial tissue is replaced with adipose tissue, resulting in decreasing T cell export from the thymus. In humans, this is thought to begin as early as 1 year of age. The rate of thymic T cell production is estimated to decline exponentially over time with a half-life of ∼15.7 years. Declining production of new naive T cells is thought to be a significant component of immunosenescence, the age-related decline in immune system function. With the recent successes of T cell-based immunotherapies, it is timely to assess how thymic involution may affect cancer and infectious disease incidence.

It is clear from epidemiological data that incidence of infectious disease and cancer increases dramatically with age, and, specifically, that many cancer incidence curves follow an apparent power law. The simplest model to account for this assumes that cancer initiation is the result of a gradual accumulation of rare "driver" mutations in one single cell. Furthermore, the fitting of this power law model (PLM) can be used to estimate the number of such mutations. Exponential curves have also been used to fit cancer incidence data, resulting in worse fits than the PLM overall. Nevertheless, it is worth noting that exponential rates close to the declining curve for thymic T cell production can be seen to emerge from the incidence data, indicating the relevance of the thymic involution timescale. While the PLM fits well, it does not account for changes in the immune system with age. To better determine the processes underlying carcinogenesis, we asked whether an alternative model, based only on age-related changes in immune system function, might partly or entirely explain cancer incidence.

Our model outperforms the power law model with the same number of fitting parameters in describing cancer incidence data across a wide spectrum of different cancers, and provides excellent fits to infectious disease data. Our hypothesis and results add to the understanding of infectious disease and cancer incidence, suggesting in the latter case that immunosenescence, rather than gradual accumulation of mutations, serves as the predominant reason for an increase in cancer incidence with age for many cancers. For future therapies, including preventative therapies, strengthening the functionality of the aging immune system appears to be more feasible than limiting genetic mutations, which raises hope for effective new treatments.

Heterochronic parabiosis involves joining the circulatory system of two animals, one old, one young, in order to observe the results. At a high level, the older individual exhibits reversal of some aspects of aging, and the young individual exhibits acceleration of some aspects of aging. The details are complex, and still debated in many cases, however. Researchers see this phenomenon as one of the more effective paths forward to identifying the important age-related changes in the environment of signals generated by cells that find their way into the bloodstream. A more effective approach would be to repair the underlying damage that causes aging - and thus also causes signaling changes - but the technologies to achieve that goal barely exist yet. Of the needed approaches, only clearance of senescent cells via senolytic pharmaceuticals is both easily studied in the laboratory and producing a great deal of useful data.

Branching out from the initial focus on joined circulatory systems, there are numerous other possible approaches to mixing young and old signals and tissues. Groups are assessing the results of transfusions of blood or plasma from young to old, for example, with Alkahest and Ambrosia as two of the more public examples. There is mixed data for the effectiveness of this strategy in comparison to parabiosis, however. The nature of the interactions when blood is circulating through two bodies is significantly different from that of even regular transfusions, and that may be important. For example, what if outcomes depend upon young tissues reacting to signals present in old blood and stepping up beneficial activities in response?

Looking further afield, we might consider investigating the transplantation of organs and other large tissue sections. The organ donation and transplant industry is, in effect, an enormous natural experiment in what happens when tissues are placed into an older or younger environment. It further has the advantage of providing human data rather than animal data. What would we expect to happen when an old organ is placed into a younger body? We might expect a degree of functional rejuvenation, and that can be measured, and the details of the biochemistry assessed. Equally, we may expect that some of the damage of aging and consequent impairment of organ function will not be reverted. Human biochemistry doesn't appear to be capable of effectively clearing persistent cross-links that stiffen tissues, for example.

The logistics of obtaining data from this experiment are not quite straightforward, however. While tens of thousands of organ transplants take place every year, and there are at least hundreds of thousands of recipients still alive, tracking down past patients and connecting them reliably with medical records is an expensive proposition. Also, the more recent data is the more interesting data. The viable approach is thus to work with medical establishments for ongoing transplant procedures and the necessary followups. In this way a fair-sized study set and database could be accumulated in a year or two. The authors of this paper have made a start on such an effort, and it is interesting to see that the narrow slice of data they elected to survey shows little rejuvenating effect when old livers are transplanted into young recipients. There is, however, a negative impact when young livers are transplanted into old recipients.

Biological age of transplanted livers

The scarcity of human donor organs in terms of availability for transplants is a renowned problem. The high request of organs moves toward an increased use of marginal donors, including organs from old or very old donors usually transplanted into younger recipients. Within the context of orthotopic liver transplants, clinical evidence suggests that livers from aged donors (≥ 70 years) do have function and duration comparable to those achievable with livers from younger donors. Paradigmatic are the cases of 26 octogenarians livers being transplanted between 1998 and 2006, 15 patients out of 26 are currently alive and 2 of those organs being centenarians.

Our team was deeply involved in an Italian national project to collect biological data to answer the question - why livers from old donors may be successfully used for transplants. The first evidence was a relative low grade of aging signs of liver donors at histological and cytological level, also including the three major proteolytic activities of proteasome, comparing young and old livers. Further, we tried to investigate the epigenetic age-related modifications in terms of liver microRNAs (miRs). We discovered that at 60-70 years of chronological age, three miRs start to increase their expression level, i.e. miR-31-5p; miR-141-3p; miR-200c-3p, and we assumed such an increase as markers of aging in human liver. When a relatively young liver was transplanted into a relatively older recipient (Δ age-mismatch average: +27 years) the expression of these miRs significantly increased in the organ (follow up after graft at 15 ± 7 months). It is interesting that we were not able to document the reverse. Indeed, when a relatively old liver was transplanted into a relatively young recipient (Δ age-mismatch average: -17 years), the expression of the three above-mentioned miRs did not change (follow up after graft at 10 ± 2 months).

On the whole, these observations suggest that in the setting of liver transplantation the aging phenotype can be "transmitted/propagated" more easily than the young phenotype via the body microenvironment. Recently, we studied the above mentioned miRs using single-miR real time-RT qPCR on blood serum samples from 34 recipients stratified on the basis of donor liver chronological age. No difference was observed, thus suggesting that the phenomenon previously found was tightly related to the organ itself without miR-specific exocytosis and changes at circulating level, at least for the identified miRs.

The biological effect of donor and recipient age-mismatch is a topic rather neglected despite its great potential, biological and clinical interest. The possibility that a centenarian liver can still function properly may suggest not only the intrinsic peculiarity of this organ (slowed down ageing; regeneration phenomena), but also the interaction with the younger recipients. This interaction was previously demonstrated in heterochronic parabiosis experiments in mice models, but deep analyses need specifically in humans, aiming at explain the reason of the variability associated with the duration of transplant.

The tissue engineering and regenerative medicine communities are too large and energetic to do more than sample their output, or note the most interesting advances that stand out from the pack. The publicity materials I'll point out here are a recent selection of items that caught my eye as they went past. Dozens more, each of which would have merited worldwide attention ten or fifteen years ago, drift by with little comment every year. The state of the art is progressing rapidly towards both the ability to build complex tissues from a cell sample, such as patient-matched organs for transplantation, and the ability to control regeneration and growth inside the body. Ultimately we may not need transplantation if native organs can be persuaded to repair themselves ... but this will likely also require significant progress towards repairing the cell and tissue damage of aging, the forms of molecular breakage that degrade regenerative capacity.

Even though the research community has progressed a long way past the capabilities of even a decade ago, there remains a longer road ahead. Transplants of cell populations are still very challenging; only a small fraction of those cells survive to take up residence and contribute over the long term. The best technology demonstrations manage 10% survival or thereabouts. Standard approaches to finding the best methodology for each cell type and situation have yet to arise. There is a lot of trial and error. Yet replacement of cell populations, reliably, and with high quality, youthful, undamaged cells, is needed to treat many of the consequences of aging. Consider the loss of dopamine-generating neurons in Parkinson's disease, for example, or the wearing down of the stem cell population responsible for generating the immune system, or the structural remodeling and weakening of the heart in response to hypertension. Removing the damage that caused those issues will not automatically restore all of the losses.

For the first time, researchers have regenerated patients' damaged lungs using autologous lung stem cell transplantation in a pilot clinical trial. In 2015, the researchers identified p63+/Krt5+ adult stem cells in a mouse lung, which had potential to regenerate pulmonary structures including bronchioles and alveoli. Now they are focusing on lung stem cells in humans rather than mice. The researchers found that a population of basal cells labeled with an SOX9+ marker had the potential to serve as lung stem cells in humans. They used lung bronchoscopy to brush off and amplify these lung stem cells from tiny samples.

In order to test the capacity of lung stem cells to regenerate lung tissue in vivo, the team transplanted the human lung stem cells into damaged lungs of immunodeficient mice. Histological analysis showed that stem cell transplantation successfully regenerated human bronchial and alveolar structures in the lungs of mice. Also, the fibrotic area in the injured lungs of the mice was replaced by new human alveoli after receiving stem cell transplantation. Arterial blood gas analysis showed that the lung function of the mice was significantly recovered.

The team launched the first clinical trial based on autologous lung stem cell transplantation for the treatment of bronchiectasis. The first two patients were recruited in March 2016. Their own lung stem cells were delivered into the patients' lung through bronchoscopy. One year after transplantation, two patients described relief of multiple respiratory symptoms such as coughing and dyspnea. CT imaging showed regional recovery of the dilated structure. Patient lung function began to recover three months after transplantation, which maintained for one year.

Scientists create functioning kidney tissue

Kidney glomeruli - constituent microscopic parts of the organ - were generated from human embryonic stem cells grown in plastic laboratory culture dishes containing a nutrient broth known as culture medium, containing molecules to promote kidney development. They were combined with a gel like substance, which acted as natural connective tissue - and then injected as a tiny clump under the skin of mice. After three months, an examination of the tissue revealed that nephrons: the microscopic structural and functional units of the kidney - had formed.

Tiny human blood vessels - known as capillaries - had developed inside the mice which nourished the new kidney structures. However, the mini-kidneys lack a large artery, and without that the organ's function will only be a fraction of normal. So, the researchers are working with surgeons to put in an artery that will bring more blood the new kidney. "We have proved beyond any doubt these structures function as kidney cells by filtering blood and producing urine - though we can't yet say what percentage of function exists. What is particularly exciting is that the structures are made of human cells which developed an excellent capillary blood supply, becoming linked to the vasculature of the mouse. Though this structure was formed from several hundred glomeruli, and humans have about a million in their kidneys - this is clearly a major advance. It constitutes a proof of principle - but much work is yet to be done."

Researchers have created a new lab-grown blood vessel replacement that is composed completely of biological materials, but surprisingly doesn't contain any living cells at implantation. The vessel, that could be used as an "off the shelf" graft for kidney dialysis patients, performed well in a recent study with nonhuman primates. It is the first-of-its-kind nonsynthetic, decellularized graft that becomes repopulated with cells by the recipient's own cells when implanted.

The researchers generated vessel-like tubes in the lab from post-natal human skin cells that were embedded in a gel-like material made of cow fibrin, a protein involved in blood clotting. Researchers put the cell-populated gel in a bioreactor and grew the tube for seven weeks and then washed away the cells over the final week. What remained was the collagen and other proteins secreted by the cells, making an all-natural, but non-living tube for implantation.

To test the vessels, the researchers implanted the 15-centimeter-long (about 5 inches) lab-grown grafts into adult baboons. Six months after implantation, the grafts grossly appeared like a blood vessel and the researchers observed healthy cells from the recipients taking up residence within the walls of the tubes. None of the grafts calcified and only one ruptured, which was attributed to inadvertent mechanical damage with handling. The grafts after six months were shown to withstand almost 30 times the average human blood pressure without bursting. The implants showed no immune response and resisted infection.

Researchers have developed a blood test that correlates well with levels of amyloid-β in the brain, offering an opportunity to reduce the cost of assessing potential therapies to treat Alzheimer's disease. Currently the only reliable methods are invasive or expensive, requiring access to cerebrospinal fluid or the use of scanning technologies. This work might be considered in the broader context of a range of studies linking amyloid-β in blood vessels and bloodstream with amyloid-β in the brain; it is thought that the relationship between amyloid-β inside and outside the brain may be a two-way street, a form of equilibrium. On the one hand that means that it might be possible to leach amyloid-β from the brain by clearing it from the cardiovascular system. On the other hand, it may be the case that increased amyloid-β in the cardiovascular system due to aging is an early source of the amyloid protein aggregates that emerge in the brain.

Researchers have developed the first blood test to detect amyloid-β protein buildup in the brain, one of the earliest hallmarks of Alzheimer's disease. The findings show that measurements of the protein and its precursors in the blood can predict neural amyloid-β deposition and could pave the way for a cheap and minimally invasive screening tool for the disease. "This study has major implications. It is the first time a group has shown a strong association of blood plasma amyloid with brain and cerebrospinal fluid."

Current methods to identify amyloid-β buildup in living people are limited to costly and sometimes highly invasive procedures, such as brain imaging with a PET scanner and spinal cord fluid extraction. So researchers set out to test whether the same information could be obtained from a blood sample. Using immunoprecipitation and mass spectrometry, the team isolated and characterized amyloid proteins in the blood from a cohort of 121 people in Japan spanning a range of cognitive function, from normal to developed Alzheimer's. They showed that blood test results could predict amyloid-β levels in the brain with about 90 percent of the accuracy achieved using PET scanning. A repeat of the approach with a validation cohort of 252 people in Australia confirmed the blood test's performance.

Such a test could one day be used to detect early signs of Alzheimer's in people with no obvious symptoms. "I can see in the future, five years from now, where people have a regular checkup every five years after age 55 or 60 to determine whether they are on the Alzheimer's pathway or not. If a person knows they are on this pathway well before the onset of any cognitive impairment some would want to alter their lifestyles. It's good to see this type of study advance, as we desperately need noninvasive and low-cost markers for Alzheimer's disease. But still, at this point it is not ready for prime time."

Why do the life spans of parents exhibit some degree of correlation with the life spans of their children? "Genetics" is probably not an acceptable answer, given present evidence for natural genetic variation to contribute comparatively little to human life expectancy in all but a few rare cases. So is it cultural, where culture influences lifestyle choices closely correlated with health, such as weight gain or smoking? Or is it due to wealth effects, for much the same reasons? If so, then why is there such variation in life expectancy within specific social groups and wealth strata? These are tough questions to answer with any reliability given snapshot data from groups within human populations. Any given large study is just a single data point in the ongoing process of analysis and debate that spans decades and the entire scientific community.

In the long run, I have my doubts that good answers will be established for this and many other questions regarding the details of natural aging today. We may never know. The urge to investigate the demographics of aging will be swept away by the advent of rejuvenation therapies such as the senolytics presently under development. All natural variations in pace of aging and life expectancy will be buried beneath the size of the gains made possible through periodic repair of the cell and tissue damage that causes aging. The data will evaporate, and different concerns will occupy the scientific community of tomorrow. After all, how many members of today's scientific community spend any time on the demographics of smallpox in populations lacking treatment options? Few indeed. It will be the same for natural aging.

Mortality, life expectancy, and age-at-death are all strongly socially structured. Despite economic growth, welfare state provisions, modern medicine and a fundamental change in disease panorama, we find a negative social gradient in mortality generation after generation. Because education, occupation, and income all predict health and survival we should also expect such characteristics in the parental generation to predict the next generation's health prospects, resulting in "inheritance of longevity". It is possible, however, that this influence from previous generations is considerably broader than that working through the children's own education, occupation, and income. Variation in mortality risk within social groups is great. To understand "inheritance of longevity" we need a conceptual framework that also identifies those within-class influences.

Already in 1934 it was suggested that the first 15 years of life could determine your mortality risk during the entire lifecourse. Similarly, the so-called DOHaD (Developmental Origins of Health and Disease) theory suggests that early life experiences is an important determinant of adult health and disease. DOHaD theory has focused on specific aetiologies and influences, such as that of foetal growth restriction on blood pressure and circulatory disease. Another, earlier school of thinking argued for more general disease-causing mechanisms. Concepts like frailty, general susceptibility, or differential vulnerability refer to individual differences in the ability to survive hardship.

Demographic concepts like frailty, epidemiological ones like general susceptibility, and psychological ones like resilience all refer to the same real-life-phenomenon: a general rather than specific vulnerability to disease. Some have stressed its social roots, while others perhaps assumed it to have a more genetic basis. Resilience, in turn, may be related to both views. It could be thought of as the opposite extreme to susceptibility/frailty on the same underlying dimension. In this study, we argue that resilience is acquired early and maintained throughout life. Resilience should therefore influence the ability to survive up to a high age and be linked to longevity, as a number of studies indeed suggest.

"Inheritance of longevity" has been discussed at length in the literature. Its precise nature is somewhat elusive. Studying the entire Icelandic population, researchers concluded that longevity was inherited within families, probably because of shared genes. Other groups, looking at twin data, concluded that genetic influences on the lifespan were minimal before age 60 and only increase after that age. On the other hand, other work has rejected any idea that mortality in old age is genetically programmed. Consistent with that view, a Swedish study of men born in 1913, found that a number of social and behavioural factors measured at age 50, but not their parents' survival, predicted longevity.

Evolutionary theorists have debated whether there is any evolutionary pressure to promote survival into old age. Nevertheless, we observe a steady lifespan extension in modern societies, especially among women, partly based on falling mortality rates across their long post-reproductive period. That children tend to live longer than their parents is likely to be determined both by what experience parents brings to the next generation, and by the improved life circumstances of the children themselves in their childhood and adult life. The importance of genetic factors for longevity, we suggest, may lie in their interaction with other factors, perhaps especially if this interaction takes place at an early age.

Any successful effort to turn back immune system aging, such as by selectively destroying malfunctioning or unhelpfully configured immune cells, and restoring the generation of new immune cells to youthful levels, should go some way to addressing all of these issues. The researchers here suggest caution on selective reversal of symptoms of immune aging, as some are beneficial adaptations, but in my opinion this shouldn't apply to efforts to address the lower level causes of immune aging. Where adaptations occur, they are adaptations to those causes, an attempt to claw back some functionality in the face of decline. That becomes moot, and the adaptation should cease, if its trigger is removed.

Aging is one of the most intricate and complex biological phenomenon. One physiological system that shows marked changes during aging is the immune system. The interest of the immune system in aging is related to the fact that this is an interacting master regulatory system that keeps the organism free of invaders, either internal or external. Since the introduction of the notion of immunosenescence, many scientists have questioned the justification for unidirectional implication of the immune system and its decreased efficiency associated with aging. Whereas some functions are indeed decreased, others are increased. Therefore; changes are not as uniform as the designation would suggest.

Accordingly, we can propose a new paradigm for dynamic immune changes with aging. We suggest that aging leads to modified/modulated responses of the immune system, making it more adapted to cope with challenges (pathogens) in a given (local) environment, and not just to an eventually terminal deterioration of the immune system. From an evolutionary perspective, this is a simple optimization of the resources of the aging body, even if it ultimately leads to pathologies and death. Immunosenescence may be necessary for an adequate response to known antigens, but detrimental for responses to new antigens in most circumstances. From this perspective, many or most age-related changes in the immune system may be desirable adaptations to the aging process, and thus no need for rejuvenation seems to be necessary.

In conclusion, most experimental data on immune changes with aging show a decline in many immune parameters when compared to young healthy subjects. The bulk of these changes is termed immunosenescence. Immunosenescence has been considered for some time as detrimental because it often leads to subclinical accumulation of pro-inflammatory factors and inflammaging. Together, immunosenescence and inflammaging are suggested to stand at the origin of most of the diseases of the elderly, such as infections, cancer, autoimmune disorders, and chronic inflammatory diseases. However, an increasing number of gerontologists have challenged this negative interpretation of immunosenescence with respect to its significance in aging-related alterations of the immune system.

If one considers these changes from an evolutionary perspective, they can be viewed preferably as adaptive or remodeling rather than solely detrimental. Whereas it is conceivable that global immune changes may lead to various diseases, it is also obvious that these changes may be needed for extended survival/longevity. Recent cumulative data suggest that, without the existence of the immunosenescence/inflammaging duo (representing two sides of the same phenomenon), human longevity would be greatly shortened.

Researchers here find a disconnect between DNA methylation patterns shown to correlate well with age and processes associated with longer telomere length. Telomeres are caps of repeated DNA at the ends of chromosomes that shorten with each cell division, a part of the mechanism limiting the life span of somatic cells. Their average length tends to shorten with age when considered across large populations in a statistical analysis, but this is a tenuous relationship that has also failed to appear in some smaller studies. Here, it seems that older ages as assessed by DNA methylation can correlate with differences in telomerase, the enzyme responsible for lengthening telomeres, that are associated with longer telomeres.

In any given individual, average telomere length as currently measured in leukocytes from a blood sample is dynamic in response to circumstances; it reflects pace of cell division and the rate at which new cells with long telomeres are generated by stem cells. Unfortunately the large degree of individual and circumstantial variation means that there is little to be meaningfully said about the present value - the information is not actionable in all but rare cases of exceptionally short average length due to disease. The epigenetic clocks derived from DNA methylation measurements are much more solid, repeatable, useful metrics, judging from the evidence to date.

In that broader context, it is interesting to find signs that these two approaches to measuring an aspect of aging are not on the same page, though I think the researchers here overstate the significance of their work and/or engage with a strawman to some degree in their comments. What they have found does fit in with the evidence to date supporting the idea that telomere length is only very loosely associated with aging, with considerable variation between individuals. That is somewhat distinct from the question of whether or not telomerase gene therapies are a useful approach to the treatment of aging or other conditions.

Researchers analyzed blood samples from nearly 10,000 people to find that genetic markers in the gene responsible for keeping telomeres (tips of chromosomes) youthfully longer, did not translate into a younger biologic age as measured by changes in proteins coating the DNA. DNA methylation age is a biomarker of chronological age and predicts lifespan, but its underlying molecular mechanisms are unknown.

In this genome-wide association study, researchers found gene variants mapping to five loci associated with intrinsic epigenetic age acceleration (IEAA) and gene variants in three loci associated with extrinsic epigenetic age acceleration. Variants in the gene called Telomerase Reverse Transcriptase (TERT) on chromosome 5 that were associated with older IEAA were also associated with longer telomeres indicating a critical role for TERT in regulating the epigenetic clock, in addition to its established role of compensating for cell replication-dependent telomere shortening.

"We calculated the epigenetic aging rate for each person using a previously described epigenetic clock method. Next, we related the epigenetic aging rate to millions of genetic locations (SNPs) across all of the chromosomes. Then we studied the SNPs that had very significant associations with epigenetic aging rates. To our surprise, one of these locations was the TERT locus. The finding is surprising because this was not a study of telomere length. TERT is a subunit of the enzyme telomerase, which is widely known because it has been touted as an anti-aging enzyme. Our study highlights the error in the notion that activation of telomerase (as advocated by some) will cure aging. Instead, our study shows that an anti-aging therapy based on telomerase expression would be accompanied by continued aging."

The research community has been devoting more time and energy to the investigation of extracellular vesicles of late. These membrane-bound packages of proteins and other molecules are an important facet of the way in which cells communicate with one another. Signaling between cells is itself very significant, a potential point of intervention for many classes of therapy. For example, most current stem cell therapies appear to work largely due to the signaling provided by transplanted cells - given sufficient understanding of the signaling, the cells could be dispensed with and the signals applied directly.

As another example, the growing presence of cellular senescence with age has a large detrimental impact on tissue function, despite the comparatively small numbers of senescent cells present even in older individuals, because these negative effects are mediated by signaling. In this way, a handful of errant cells can put the entire local environment into disarray. On that topic, the open access paper here takes a short tour of what is known about extracellular vesicles in the context of cellular senescence.

Cellular senescence prevents the proliferation of cells exposed to potentially oncogenic stresses, such as DNA-damaging reagents, irradiation, telomere shortening, and oncogene activation. Mutations in genes essential for the senescence-induced cell cycle arrest predispose cells to immortalization and shorten lifespan by increasing cancer incidence. However, cellular senescence not only arrests the cell cycle but also changes how the cell impacts its microenvironment. The way in which senescent cells influence their microenvironment is highly context dependent. It promotes tumor development in many cases, but can also be tumor suppressive in certain circumstances. Removal of senescent cells that accumulated in the body during aging alleviates atherosclerosis, hepatic steatosis, tumor development, and functional declines of heart, kidney, and fat tissues, resulting in prolonged healthspan and lifespan. These effects may be attributable to so-called , whereby cells secrete high levels of inflammatory cytokines, chemokines, growth factors, and metalloproteinases.

Although the involvement of typical secretory proteins in the non-cell-autonomous effects of senescent cells has been well studied, the functions of membrane-enclosed vesicles secreted by senescent cells have not been studied until recently. These extracellular vesicles (EVs) were once thought to be cellular trash, but now it is clear that they are critical mediators in intercellular communication. Emerging evidence indicates that EVs also play important roles in cellular senescence and aging. This field is rapidly advancing especially since it was reported that EVs deliver functional RNA to the recipient cells. Extracellular vesicles contain a huge variety of proteins and nucleic acids in a cell type-dependent manner.

Senescence-associated increase in EV secretion seems to be a general feature of cellular senescence and has been observed in fibroblasts, epithelial cells, and cancer cells. This increase is at least partially mediated by p53 and one of its targets, TSAP6, although the mechanism whereby TSAP6 regulates EV secretion is not well understood. It is known that EV secretion contributes to the clearance of harmful molecules in cells, such as cytoplasmic DNA. It has been shown that EV-mediated removal of cytoplasmic DNA is essential for the survival of senescent cells, which may explain why EV secretion is increased in senescent cells.

Recent findings implicate senescent cell EVs in cancer development, vascular calcification, and age-related decline in bone formation. Increased secretion of EV-associated DNA from senescent cells is likely to be pro-inflammatory and may contribute to age-related chronic inflammation. Whether senescent cell EVs promote or suppress cancer development may be context dependent. Despite this progress, it should be noted that the functions of senescent cell EVs are still understudied, at least partially due to inadequate understanding of EVs themselves. This research field is immature and the methods used are not sufficiently standardized yet. Nevertheless, EVs are now shown to be critical players in cellular senescence and aging, and more functions will be revealed in the future as the EV research field matures.

Here, researchers examine the correlation between ventricular dsyfunction, other noted forms of damage observed in brain aging, and the onset of cognitive decline. The ventricular system is where cerebrospinal fluid is created and circulates throughout the brain. Many things go wrong in the aging brain, all stemming from the same few root cause processes of damage accumulation in and around cells. Thus correlations between specific observed changes and the progression of dementia should be expected, but don't necessarily imply direct causation - though a particularly good correlation always indicates that further investigation is probably merited.

This line of investigation ties in to a growing area of research regarding the impairment of drainage of cerebrospinal fluid in aging. This impairment may explain the slowly rising levels of protein aggregates and other molecular waste in the brains of older individuals, a state of affairs known to contribute to the development of neurodegenerative conditions. Normally these wastes are removed at some pace through various filtration and drainage channels for cerebrospinal fluid, but the channels become dysfunctional, just like all other biological systems in older individuals. Leucadia Therapeutics is an example of a company working to intervene and restore youthful levels of drainage to what they consider the more important path. Other groups are looking into different areas of impaired fluid flow in the brain. All in all it is a most interesting and promising area of development.

The human brain's ventricular system is essential for the movement of nutrient-rich cerebrospinal fluid (CSF) throughout the central nervous system. A special epithelial lining along the ventricle walls composed of ependymal cells allows for the movement of CSF nutrients into the brain parenchyma as well as clearance of proteins and metabolites from the interstitial fluid (ISF). This ependyma-mediated bidirectional CSF-ISF exchange, as well as the formation of a cell barrier to prevent movement of proteins and metabolites from the CSF back into the ISF, relies on the presence of an intact ependymal cell monolayer. Pathological conditions in humans that are characterized by ependymal cell stretching and/or loss, including hydrocephalus, typically result in decreased CSF turnover rates and impaired clearance of proteins and metabolites resulting in a harmful buildup of these substances in brain parenchymal tissue.

Longitudinal magnetic resonance imaging (MRI)-based studies have established that expansion of the brain's fluid-filled lateral ventricles (LVs), or ventriculomegaly, is a defining feature of the aging brain. Ventricle expansion rates correlate strongly with declining cognitive performance and the rate of ventricle volume increase has been linked to an increase in Alzheimer's disease (AD)-related amyloid-beta (Aβ) plaques and tau neurofibrillary tangles, as well as alterations in CSF biomarker composition. Together, these point towards defective CSF-ISF exchange and impaired clearance mechanisms that are characteristic of AD.

Degeneration of periventricular brain tissue and declines in associated white matter tract integrity are common with normal aging and the extent of periventricular tissue abnormalities has been linked to dementia and AD. Periventricular hyperintensities (PVH), as measured using MRI, are indicative of fluid accumulation, or edema, often located in the parenchymal tissue directly adjacent to the frontal and occipital horns of the LV. The precise etiology of PVH is not clear; however, studies have implicated impaired drainage of ISF from the periventricular white matter resulting in aberrant fluid accumulation.

In previous studies, we found that enlarged ventricles from aging humans exhibited regional gliosis in the place of functional ependymal cell coverage. We predict that replacement of the ependymal lining with stratified layers of astrocytes at the ventricle surface adversely affects CSF/ISF bulk flow mechanisms, leading to fluid accumulation or edema and harmful buildup of proteins and metabolites in the periventricular space. Due to the rarity of longitudinal MRI data sets and associated subject-matched periventricular tissue biospecimens, this has never been directly demonstrated.

Using data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) and the Baltimore Longitudinal Study of Aging (BLSA), we investigated the relationships among the following variables: ventricle expansion, PVH, periventricular white matter tract integrity, and degree of cognitive impairment. We also investigated the histopathological correlates of these measures, including LV wall gliosis and periventricular protein accumulation. We found that both LV and PVH volumes increase with age, and this expansion is more rapid and dramatic in cognitively impaired (CI) subjects. We also found a direct relationship between LV volume and PVH volume increase. Case studies from the BLSA allowed us to link ventricle expansion with regional gliosis, where an intact ependymal cell monolayer was replaced with stratified layers of astrocytes in regions of LV expansion. Additionally, adjacent parenchymal regions exhibited edema (as indicated by PVH), white matter deterioration, decreased vascular integrity, and harmful buildup of proteins including Aβ and tau.

Naked mole-rats are distinguished by an exceptionally long life span in comparison to similarly sized rodents, and a near immunity to cancer. Unlike other mammals, their mortality rates stay fairly constant until very late life. They accumulate all the signs of significant oxidative damage in cells and tissues, but seem resilient to it. Similarly, researchers here note that naked mole-rats do in fact accumulate senescent cells, one of the root causes of aging, but appear resilient to the harmful presence and activities of these cells. Exactly why this is the case has yet to be determined.

Cells become senescent in response to potentially cancerous damage or reaching the Hayflick limit on replication. The vast majority destroy themselves or are destroyed by the immune system, but a tiny fraction linger. They generate signals that spur chronic inflammation, change surrounding cell behavior for the worse, and destructively remodel nearby tissue structures. This results in functional decline in organs and other important tissues and systems. It is interesting to see that while there are differences in the detailed behavior of senescent cells between naked mole-rats and other mammals, they nonetheless still generate the same damaging signals, and yet the naked mole-rats appear to shrug it off.

With their large buck teeth and wrinkled, hairless bodies, naked mole rats won't be winning any awards for cutest rodent. But their long life span - they can live up to 30 years, the longest of any rodent - and remarkable resistance to age-related diseases, offer scientists key clues to the mysteries of aging and cancer. That's why researchers studied naked mole rats to see if the rodents exhibit an anticancer mechanism called cellular senescence.

Previous studies indicated that when cells that had undergone senescence were removed from mice, the mice were less frail in advanced age as compared to mice that aged naturally with senescent cells intact. Researchers therefore believed senescence held the key to the proverbial fountain of youth; removing senescent cells rejuvenated mice, so perhaps it could work with human beings. But is eliminating senescence actually the key to preventing or reversing age-related diseases, namely cancer?

Researchers compared the senescence response of naked mole rats to that of mice, which live a tenth as long - only about two to three years. Their unexpected discovery? Naked mole rats do experience cellular senescence, yet they continue to live long, healthy lives; eliminating the senescence mechanism is not the key to their long life span. The researchers found that although naked mole rats exhibited cellular senescence similar to mice, their senescent cells also displayed unique features that may contribute to their cancer resistance and longevity.

The cellular senescence mechanism permanently arrests a cell to prevent it from dividing, but the cell still continues to metabolize. The researchers found that naked mole rats are able to more strongly inhibit the metabolic process of the senescent cells, resulting in higher resistance to the damaging effects of senescence. "In naked mole rats, senescent cells are better behaved. When you compare the signals from the mouse versus from the naked mole rat, all the genes in the mouse are a mess. In the naked mole rat, everything is more organized. The naked mole rat didn't get rid of the senescence, but maybe it made it a bit more structured."

Researchers here find that the longest lived bats have unusual telomere biochemistry, and in fact unusual enough that the new knowledge may turn out to be of little relevance to the understanding of telomeres, telomerase, and aging in other mammals. It appears that they rely upon alternative lengthening of telomeres (ALT) to maintain telomere length, a process that doesn't operate in any normal adult human cell. Given that loss of telomere length appears to be a marker of aging rather than a cause, and a fairly loosely coupled marker at that, the real relevance of this area of biochemistry probably lies in the relationship between telomerase and important cellular activities, such as ability and willingness of somatic cells to replicate, or stem cells to support tissue function.

Bats exhibit cellular biochemistry that is somewhat different from that of ground-based species in a number of other ways. The metabolic demands of flight have led to, for example, greater resilience to stress and damage arising from the normal operation of cellular metabolism. When charting life span against metabolic rate, where high metabolic rates usually imply short life spans, some small bat species are noteworthy outliers. Brandt's bat, for example, has a life span of four decades despite being the same size as ground-dwelling mammals that live for only a couple of years.

One of the principal caveats at the present stage of research into telomeres and the use of telomerase gene therapies - or other means of enhancing telomerase activity - as a treatment for aspects of aging is that mice and humans have quite different telomere dynamics and patterns of natural telomerase activity. The balance between cancer risk and beneficially increased stem cell activity resulting from telomerase therapies may turn out to be significantly different in different species. That these bats have their own unique evolved dynamics, ones that are much further removed, suggests that this portion of the comparative biology might not be as useful to the practical science of aging as hoped. The fastest path to understanding is probably to extend present work on telomerase therapies to species more like humans in their telomere biology, such as dogs and pigs perhaps. Or, as some advocate, running human trials immediately.

We urgently need to better understand the mechanisms of the aging process, with a view to improving the future quality of life of our aging populations. Most aging studies have been carried out in shorter-lived laboratory model species, given the ease of manipulation, housing, and length of life span. Although they are excellent study species, it is difficult to extrapolate experimental findings in these short-lived laboratory species to long-lived, outbred species such as humans. Therefore, it has been argued that long-lived, outbred species such as bats may be better models to investigate the aging processes of relevance to people.

Only 19 species of mammal are longer-lived than humans in proportion to their body size, and 18 of these species are bats. Bats are the longest-lived mammals relative to their body size, with the oldest bat recaptured (Myotis brandtii) being more than 41 years old, weighing ~7 g, and living ~9.8 times longer than predicted for its size. Although an excellent model species to study extended healthspan, logistically, it is difficult to study aging in bats because they are not easily maintained in captivity. Here, uniquely drawing on more than 60 years of cumulative long-term, mark-recapture studies from four wild populations of long-lived bats, we determine whether telomeres, a driving factor of the aging process, shorten with age in Myotis myotis (n = 239; age, 0 to 6+ years), Rhinolophus ferrumequinum (n = 160; age, 0 to 24 years), Myotis bechsteinii (n = 49; age, 1 to 16 years), and Miniopterus schreibersii (n = 45; age, 0 to 17 years).

We show that telomeres shorten with age in Rhinolophus ferrumequinum and Miniopterus schreibersii, but not in the bat genus with greatest longevity, Myotis. As in humans, telomerase is not expressed in Myotis myotis blood or fibroblasts. Selection tests on telomere maintenance genes show that ATM and SETX, which repair and prevent DNA damage, potentially mediate telomere dynamics in Myotis bats. Twenty-one telomere maintenance genes are differentially expressed in Myotis, of which 14 are enriched for DNA repair, and 5 for alternative telomere-lengthening mechanisms. These results, coupled with differential expression of ATM, SETX, MRE11a, RAD50, and WRN across all tissues in the genus Myotis compared to other mammals, suggest a potential role for alternative lengthening of telomeres (ALT) mechanisms in the maintenance of telomeres in these species. If telomeres are maintained by ALT mechanisms in Myotis species, then these genes may represent excellent therapeutic targets given that cancer incidence in bats is rare.

A fair number of the scientists working towards therapies to address cellular senescence, one of the causes of aging, are more interested in suppressing signaling from these cells than in destroying them. Cynically, a treatment one has to keep using consistently is much more interesting to pharmaceutical companies than a treatment that only has to be applied once every few years at most. Until researchers encounter a population of senescent cells that cannot be safely removed, destruction continues to look like the far better option. Senescent cells are harmful because of the mix of signals they generate, a mix that is still comparatively poorly mapped and understood. Suppressing it may well prove to be a lengthy and difficult process of progress by small degrees, while destruction can be achieved in the near future and removes all of the harmful signaling whether or not it is understood.

Astrocytes are one potential candidate for a population of senescent cells that might be challenging to remove. It isn't completely clear that all of the astrocytes showing markers of senescence are actually senescent, but if so it represents a large portion of all astrocytes in the aging brain. Abrupt clearance of these cells would probably not be healthy, regardless of the incremental harms they are causing. With this sort of thing in mind, it is prudent to have a backup strategy under development, whether that is some form of careful incremental winnowing and replacement of these cells over time, or a form of suppression of their bad behavior while allowing them to live.

One of the common features of aging is low-level chronic inflammation, termed sterile inflammation or inflammaging. Even though all the sources of inflammaging are unclear, it likely derives at least partly from senescent cells. Mammalian cells undergo senescence in response to stressful stimuli. An important feature of senescent cells is the secretion of a myriad of biologically active factors, termed the senescence-associated secretory phenotype (SASP).

The SASP is similar between mice and humans, and comprises inflammatory cytokines such as IL-6 and IL-8. The SASP can disrupt the surrounding microenvironment and normal cell functions, and stimulate malignant phenotypes in nearby cells. Senescent cells can also promote tumor growth in mice. Because senescent cells increase with age and are frequently found within hyperplastic and degenerative tissues, the SASP may be a major cause of inflammaging. Compounds that modulate the SASP hold promise for ameliorating a number of diseases of aging, including cancer.

Nutlins were originally identified as potent small molecules that inhibit the interaction between p53 and MDM2, which promote p53 degradation. Nutlin therefore stabilizes p53, thereby promoting the apoptotic death of cancer cells. Importantly, in cancer cells, nutlin-3a inhibits the activity of NF-κB, a potent transcriptional stimulator of genes encoding inflammatory cytokines, in a p53-dependent manner. The clinical importance of small-molecule MDM2 inhibitors like nutlin-3a spurred the discovery of similar compounds, such as MI-63, which are more efficient inhibitors of the MDM2-p53 interaction.

We investigated the effects of small-molecule MDM2-p53 interaction antagonists on senescent phenotypes, including the SASP, of primary human fibroblasts and epithelial cells. We used nutlin-3a, as well as the non-peptide small molecule inhibitor of MDM2, MI-63. We compared these compounds for their ability to induce a growth-arrested state, whether quiescence or senescence, in human cells, and evaluated their ability to modulate the SASP. We found that both compounds trigger selected markers of a senescent-like state, but the growth arrest was reversible, and both significantly suppressed the SASP, suggesting potential utility as therapeutic agents.

Oxidative damage has long been linked to aging, but the general use of antioxidants does nothing for life span. In fact, the evidence suggests this approach is modestly harmful, possibly due to blocking the oxidative signaling needed for exercise and other, similar mild stresses to produce benefits via hormesis. Antioxidant compounds targeted to the mitochondria are a different story, however, and have been shown to slow aging or partially reverse some aspects of aging in mice and lower animals - as is the case in this open access paper.

Mitochondria are the power plants of the cell, and generate reactive molecules that raise oxidative stress as a side-effect of the processes that produce chemical energy stores. This flow of reactive molecules influences the behavior of the cell in numerous ways; methods of slightly slowing aging have been demonstrated that either lower production, leading to less oxidative damage, or raise it, spurring increased maintenance activities in the cell. In the research here, benefits are derived indirectly: damping down oxidative damage improves the function of blood vessels in the aged brain, which helps to restore some degree of lost cognitive function in old mice. The brain is an energy-hungry organ, and age-related neurodegenerative conditions are characterized by a general decline in the capacity of of the blood supply and mitochondria in cells to supply as much energy as is needed.

Normal functioning of the central nervous system (CNS) requires a continuous, tightly controlled supply of oxygen and nutrients as well as washout of harmful metabolites through uninterrupted cerebral blood flow (CBF). The energetic demands of neurons are very high, yet the brain has very little energetic reserves. During periods of intense neuronal activity, there is a requirement for adjusting oxygen and glucose delivery to local neuronal activity through rapid adaptive increases in CBF. This is ensured by a mechanism known as neurovascular coupling (NVC). The resultant functional hyperemia is a vital mechanism to maintain optimal microenvironment of cerebral tissue and thereby ensuring normal neuronal function.

There is an increasing appreciation that (micro)vascular contributions to cognitive impairment and dementia in elderly patients are critical. Importantly, neurovascular coupling responses are impaired both in elderly patients and aged laboratory animals. Experimental studies support this concept, showing that pharmacologically induced neurovascular uncoupling in mice mimics important aspects of age-related cognitive impairment. On the basis of these findings, we proposed that novel therapeutic interventions should be developed to rescue functional hyperemia in elderly patients to prevent/delay cognitive impairment. Previous studies demonstrate that aging exacerbates generation of reactive oxygen species (ROS) in the cerebromicrovascular endothelial cells, which contribute to age-related neurovascular uncoupling in aged mice by promoting endothelial dysfunction. We hypothesize that pharmacological treatments, which attenuate endothelial oxidative stress, will have the capacity to improve neurovascular coupling in aged individuals.

The mitochondrial free radical theory of aging posits that mitochondria-derived ROS (mtROS) production and related mitochondrial dysfunction are a critical driving force in the aging process. In support of this theory, it was demonstrated that attenuation of mitochondrial oxidative stress (by mitochondria-targeted overexpression of catalase) increases mouse lifespan. There is particularly strong evidence that mitochondrial oxidative stress is implicated in cardiovascular aging processes. Yet, although drugs that improve mitochondrial function have been shown to exert beneficial effects both on the vasomotor function of peripheral arteries, their potential protective effects on the aged cerebral microvasculature has not been investigated.

This study was designed to test the hypothesis that pharmacological attenuation of mtROS can restore cerebromicrovascular endothelial function and thus improve neurovascular coupling in aged mice. To achieve this goal, in aged mice mitochondrial oxidative stress was manipulated by treatment with the mitochondrial-targeted peptide SS-31. We found that neurovascular coupling responses were significantly impaired in aged mice. Treatment with SS-31 significantly improved neurovascular coupling responses by increasing cerebromicrovascular dilation, which was associated with significantly improved spatial working memory, motor skill learning, and gait coordination. These findings are paralleled by the protective effects of SS-31 on mitochondrial production of reactive oxygen species and mitochondrial respiration in cultured cerebromicrovascular endothelial cells derived from aged animals.

Is Gut Bacteria Making You Fat? There are millions of bacteria that inhabit our guts. Most are beneficial, and are referred to as Probiotics. A healthy and diverse population of these good bacteria are key to proper functioning of our digestive and immune systems, greatly impacting our physical and mental health. (1, 2, 3, 4). We can improve the population …

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Wed Jun 12 17:36:16 PDT 2013

What is LongeCity?
LongeCity is a registered, members-based non-profit organisation. More info here.

What THEMES of science projects does LongeCity support?
We support research into ageing and the extension of human lifespan. This means we support many types of medical research and research into basic biology, but there should be an angle that will allow people to live longer, healthier lives.

What TYPES of science projects does LongeCity support?
We support laboratory research, clinical research, bioinformatics and theoretical research in the ‘hard sciences’. We do not normally support social science research.
We do support some events, mentorship and travel to scientific conferences, but not under the ‘research budget’.

Where can the research take place?
Anywhere in the world. Laboratory research should normally be conducted in an established lab.

What does LongeCity expect in return?
Scientific integrity. Normally a written report. Interim updates for longer projects. Acknowledgement of the funding received. We may approach previous grantholders to be available as peer reviewers for future research applications.

What grant schemes are available?

a) Small GrantsFunding: up to $500Who can apply: any LongeCity Member, it helps if you have a sponsor/supervisor with some track recordType: typical cases are support for summer projects, internships, workshops, review paper writing, selected consumables Next deadline: none, applications are welcome until the annual budget is exhaustedDetails: http://www.longecity...s/action/grants

b) Matching FundraiserFunding: up to $20.000 (in total- matching fundraiser)Who can apply: ScientistsType: For selected projects, LongeCity will issue a call for donations and for every dollar received LongeCity will match (or better) the donation. The entire money goes to support the research project. Next deadline: July 1st 2013Details: http://www.longecity...ts/research2013

by josh mittledorf @ Alivebynature – Evidence Based Reviews

Sat Jan 20 10:39:49 PST 2018

Life Extension Foundation has just announced that next week they are going to announce a partnership with the Young Blood Institute for what is perhaps the most ambitious human trial of anti-aging medicine ever. It’s a daring project, with what is IMO a most promising target. But I find details of their protocol puzzling, and […]

by undefined @ Canadian CattlemenCanadian Cattlemen

Tue Feb 06 08:16:26 PST 2018

Canadian Cattlemen’s Association (CCA) leadership travelled to two major agriculture policy conventions in the United States in early January to promote common interests in the North American Free Trade Agreement (NAFTA) and urge progress on regulatory modernization to improve the flow of trade between the two countries. The advocacy efforts are part of an increasingly […] Read more

by undefined @ Canadian CattlemenCanadian Cattlemen

Mon Apr 03 13:05:49 PDT 2017

A number of times over the years I have been asked the question “do cattle feel pain the same way we do?” To answer the question, it’s important to understand a little bit about pain physiology. When a pain stimulus is administered to an animal (for example, you pinch the claw on the hind leg […] Read more

by @ LongeCity - Articles

Tue Jan 08 11:39:43 PST 2013

There are 4 ways of writing for LongeCity:

(1) Commissioned topics
800-1500 word (ca. 2-3 pages) articles on any of the topics listed below.
As long as the topic is listed, it remains open for submissions.
Authors are invited to submit a finished manuscript directly to caliban@longecity.org. Responses can be expected with 14 days after submission.
Editors may require certain alterations for style, quality or based on
peer-reviewed references, but publication is guaranteed for commissioned
articles if the article meets a basic quality threshold.

(2) Submit an exposé for a new topic
You can send us a 200 word article outline, accompanied with a few lines about
yourself. If accepted, you will be invited to submit a full article.
Please use the contact form.

Reward per published article: $180 (a premium may be awarded for particularly well-researched articles)

(3) Write a blog or (4) write on the forum
You can either start a blog at LongeCity or easily synchronise a blog that you
maintain elsewhere. If your blog is consistently of interest and of good
quality, you will automatically be awarded ‘Thank You’ points which can be
redeemed for vouchers at online stores such as amazon. We might also ask you to
do a regular column.
Thank you points also accrue to forum posts, as readers 'like' your posts.

All articles and other written contribution are subject to the general LongeCity
User agreement. In short authors keep full copyright of the article, but grant a
free perpetual and worldwide license to LongeCity for non-commercial use.

by Ken Silvers @ Probiotics Center

Wed Nov 08 22:01:59 PST 2017

The Turmeric Ginger Latte is a favourite drink for many. And no wonder, it’s absolutely delicious! The main ingredients, turmeric and ginger, are potent cousins working extremely well together. And the list of turmeric’s and ginger’s health benefits seems never-ending. It also includes many gut and digestive problems. Turmeric Ginger Latte benefits The Turmeric Ginger Latte combines two […]

by @ Articles - Articles

Fri Nov 18 13:03:14 PST 2011

by Sven Bulterijs & Paul McGlothin,

Often described as the only proven intervention that extends mean and maximal life-span in mammalian species, it is also a lifestyle choice for the committed immortalist. But why and how does it work? How to begin and what are the downsides?

These and other questions are dressed in a short feature by Paul McGlothin, Co-author of “The CR Way” andin a voiced slideshow by Sven Bulterijs, LongeCity Director and student in biochemistry and biotechnology.

by Owen Alexander @ Alt Protein

Sat Dec 30 11:02:30 PST 2017

For many fitness fanatics, consuming pre-workout supplements are something of a ritual. Such people view the consumption of pre-workouts before hitting the gym to be absolutely essential. To them, not consuming pre-workout will only lead to a low energy, low results workout. At the same time, there is a significant segment of the fitness population ... Read moreGarden of Life Energy and Focus Review That You’ll Love

by Owen Alexander @ Alt Protein

Tue Jan 23 19:52:05 PST 2018

is a popular product among protein powder fans. The entire community of athletes and fitness enthusiasts like these shakes. One of their major advantages is the large array of available flavors and formulas. This supplement brand has launched a wide range of drinkable formulas so there are plenty of options to choose from. This way, ... Read moreThe Top 7 Best MyProtein Flavors to Consider in 2018

by @ LongeCity - Articles

Tue Dec 18 15:30:56 PST 2012

Visitors to the forum will notice that a lot of discussion evolves around nutrition, supplements and lifestyle. We realize of course that these factors are just one element of the larger mission to conquer the blight of involuntary death, but that makes it all the more important to make sure that the strengths that LongeCity has in providing a great resource for nutritional information exchange
are leveraged effectively.

Sometimes, it may seem like there are two 'factions' at LongeCity: on the one hand the committed 'activists' who realize the truth that nutritional supplements by themselves will have very limited efficacy in extending the human lifespan and who consequently have little patience for 'supplement pushers'. On the other hand there are the 'supplementers' who have little to no interest in 'living forever' and whose priority is a healthy lifespan and enhancing their fitness. For sure, examples of both 'camps' can be found if one looks for them, but on the whole the distinction has very little merit: firstly, nutrition, drugs, vitamins and lifestyle - even apparently peripheral topics like cognitive enhancement, are an important factor in the portfolio of life extension technologies. These are the factors that we can do for ourselves, today and for that reasons alone are worth discussing.

This fact- that supplements are at the 'applied' end of life extension discussion also means that the information and expertise joining at LongeCity around supplements can be much more effectively leveraged for fundraising. This makes LongeCity pretty unique: we are trying to siphon some of the financial overheads from the commercial end of life extension and re-allocate them to chronically underfunded scientific research and advocacy programmes. LongeCity has been really successful in this regard: with very little funding we have made a real difference in creating pioneering information material and funding important basic research as well as supporting community projects.

Thus 'activists' can appreciate a measure of advertising at the sitefor making an important contribution to the common cause. Ad exposure for Members is reduced but not fully eliminated not least because we think that some ads can actually be useful and interesting. There are at least four types of advertising available:

'Google ads' - are context-related ads. Google offers these individually based on your browser's settings and the content of the forum. Consequently please bear in mind that LongeCity has very limited control about what ads are displayed.

'Banner ads' - these paid for adverts usually leading to a sponsors website. More about LongeCity's relationship with other institutions can be found in this article. To quote: "LongeCity does not endorse any advertisers beyond the fact that they have made a donation to the community in exchange for exposure. Advertisers never influence our policy, ever. (...) Having said that, advertisers featured at LongeCity very often have a real commitment to the cause- they would not have found us otherwise". Members are invited to comment on the policy

'Links' - these are links in text and elsewhere that are monetized if the link is used to make a purchase at the external site. One well known example is Amazon.com: If you use the LongeCity 'referral' page to make a purchase, Amazon makes a small payment to LongeCity at no cost to you. We may be experimenting with other link concepts in the future. Note however, that the connections on our links page are not used in this manner. They are simply a project index interesting sources that all members can contribute to.

'Ads by discussion' - sometimes advertising momentum is generated simply by discussing a particular product. Over the years, marketers have become very sophisticated in pursuing such 'viral' strategies - and they are generally NOT WELCOME at LongeCity. There are only two sub-forums where product-and vendor related discussions are tolerated: for supplement companies/ for other companies. Any attempts to initiate product-related discussions elsewhere will be considered a breach of the LongeCity user agreement. The limited discussion that is allowed in this context is tolerated only because we feel that some information exchange about products and providers is potentially part of the LongeCity mission. Where this link cannot be made clearly, ads by discussion -whether inadvertent or not- will not be permitted.

We have experimented a little bit and are always keen to find other ways to generate funding for life extension research and advocacy from the LongeCity website in a way that is not overly intrusive and that does not compromise our mission and values.
Potential sponsors are invited to get in touch.
Members with new ideas about are invited to share them in the suggestions forum .

by admin @ Alivebynature – Evidence Based Reviews

Sat Jan 20 16:10:53 PST 2018

By Stephen Harrington Scientists are discovering new ways that NAD+ facilitates healthy longevity.1-3 NAD+ levels markedly decline with age, creating an energy deficit that decreases the body’s ability to retain youthful function.4 To give you an idea how impactful NAD+ can be, by age 50 a typical person may have only half the NAD+ they […]

by @ CTVNews.ca - Top Stories - Public RSS

Mon Feb 12 13:14:00 PST 2018

The grieving relatives of a First Nations man whose accused killer was acquitted by a Saskatchewan jury are meeting with federal ministers to take what they call a first step in the long road to reforming Canada's justice system.

by admin @ Alivebynature – Evidence Based Reviews

Thu Feb 01 08:26:47 PST 2018

Whether you are a athletes looking to improve performance or Mother looking to lose stubborn fat. How you eat is part of that equation. CrossFitters are no exception. The Paleo (Paleolithic) diet is one that has been adopted by many for that reason.The Paleo diet involves eating all natural foods and avoiding processed ones. Let’s look at what the […]

by Owen Alexander @ Alt Protein

Tue Jan 23 13:12:43 PST 2018

When it comes to whey protein supplements, the most basic fitness supplement there is, you won’t be lacking for choices. For such a simple and relatively undifferentiated product, you have literally hundreds of options to choose from. So it’s no surprise that most consumers stick to the most popular choices such as Optimum Nutrition Gold ... Read moreThe Bluebonnet Whey Protein Isolate Review- Is it worth it?

by @ Articles

Tue Jul 18 14:03:16 PDT 2017

Sven Bulterijs continues his discussion of prominent compounds with potential life extension efficacy by looking not just at rapamycin but also at its target, the mTOR pathway, which has likely a key role in mediating lifespan.
⇒ read the article in "Sven's Science Corner" blog

by @ Articles - Articles

Tue Feb 21 13:06:47 PST 2012

The following is a quick overview on Cryonics.

NB: The information below is periodically reviewed for accuracy, but LongeCity makes no representations or gives any warranties whatsoever that the following information is accurate and complete at any point in time. LongeCity accepts no responsibility or liability for information contained on this page. The discussion of cryonics service providers and services in no way entails any endorsement on part of LongeCity. The lead author of this page, its editors and other contributors from time to time may be affiliated with one of the service providers mentioned below. Without qualification to the foregoing disclaimers, LongeCity strives to present the following information in an objective and balanced manner. If you feel that information on this page is inaccurate or imbalanced please contact the LongeCity Support Email.

Cryonics is based on the idea that future medicine will have capabilities well beyond those of current medicine, including the ability to cure all diseases, rejuvenate and repair damage incurred in the cryopreservation process — through the use of nanotechnology and other technologies. Cryonics can be an ambulance or time capsule to future medicine which can allow us to live many thousands of years or longer in youth and good health. Stored at very low temperatures there will be very little molecular motion in cryonics patients for tens of thousands of years, although most of us do not believe that we will have to wait anywhere near so long for future medicine.

Although cryonics patients must be legally dead before cryonics procedures to reduce or eliminate ischemic damage and ice formation can be applied, cryonicists do not believe that cryonics patients are dead in an ultimate sense. Nearly all the cells of the body are alive for quite some time after the heart stops — including neurons. A standby team can be used to minimize the time between pronouncement of death and cooling, cardiopulmonary support, etc. Cryonicists believe that the anatomical basis of mind can survive much longer than six minutes after stoppage of the heart in the absence of cooling — despite the inability of current medicine to revive patients without neurological damage after more than six minutes of cardiac arrest. (See Quantifying Ischemic Damage for Cryonics Rescue for more details.)

Existing Cryonics Organizations

For most of cryonics history (which began in the mid-1960s), all of the cryonics organizations offering cryonics services have been in the United States. In 2005 a cryonics organization was created in Russia (just northwest of Moscow) and there are plans for another cryonics organization in Australia to offer perfusion and storage of cryonics patients within a few years. LongeCity does not endorse any particular cryonics organization. The data below is taken from the cryonics organizations without LongeCity attempting to verify the accuracy of their claims or the extent of the services they claim to provide. If you are considering utilizing any of these organizations, you should conduct your own investigation.

Oregon Cryonics was incorporated in 2005, but accepted its first patient (a pet patient) in May, 2014. Jordan Sparks is the owner/operator, but he has plans for a Board of Directors or other mechanism to out-live him (to allow for the organization to continue).

Cryonics Services Offered

Not all cryonics services are offered by all cryonics organizations. Patient administration service is offered by cryonics organizations that sign-up Members who are to be cryopreserved upon legal death and maintain responsibility for those Members while they are Patient's in cryopreservation storage. Perfusion is the replacement of normal body fluid with cryoprotective solutions to reduce or prevent ice formation at cryogenic temperatures. Storage is the storage of a cryonics patient in liquid nitrogen. Standby/Stabilization/Transport (SST) involves standing by the bedside of a medically terminal patient destined to be cryopreserved, the application of a heart-lung resuscitator and ice-water cooling as soon as possible after declaration of death,and transport to a perfusion facility while tissues are still being stabilized at low temperature.

The following table represents the services which cryonics organizations say they provide.

NAME

PATIENT ADMINISTRATION

PERFUSION

STORAGE

SST

Alcor

Yes

Yes

Yes

Yes

ACS

Yes

Yes*

No*

Yes*

CI

Yes

Yes

Yes

No*

KrioRus

Yes

Yes

Yes

No

Oregon Cryonics

Yes

Yes

Yes

No

SA

No*

No

No

Yes

Trans Time

Yes

No

Yes

No

*=simplification, see explanation

All standby cases done for Alcor Foundation outside of Arizona, but inside the continental United States are handled by Suspended Animation, Inc (SA). Alcor does standby for Alcor Members who are terminal in Arizona, Hawaii, and Alaska as well as in Canada. SA does not provide SST services outside the continental United States for any organization.

The American Cryonics Society (ACS) states that it mainly contracts with Suspended Animation,Inc. (SA) for perfusion and standby/transport, and contracts with the Cryonics Institute (CI) for storage. ACS also states that it has equipment, contractors and volunteers which are available for use in perfusion and standby in California should the need arise, although this is far less sophisticated and formal than what SA provides. ACS creates and manages individual charitable trusts for its patients. ACS regards these trusts as an important feature of the benefit gained by being an ACS Member.

Cryonics Institute (CI) Members who reside in the continental United States have the option of contracting directly with SA if they desire professional SST.In some cases volunteers or paid funeral directors have provided these services to CI Members. SA will keep records of CI Members who have arranged to have SA SST, but does not continue any administrative responsibility after the patient has been cryopreserved.

Trans Time is currently storing patients, but (despite what their website says) is not currently seeking new Members or Patients.

Sizes of the Organizations

There are various ways by which organization size could be measured, but for the purposes of this section size is represented by the number of Members in the organization, the number of patients currently being stored in liquid nitrogen and the number of full-time paid staff in the organization. The figures below are for April 2017, and are based on the statements of the organization in question.

NAME

MEMBERS

FUNDED MEMBERS

PATIENTS

STAFF

Alcor

1,639*

1,132*

150

9*

ACS

?*

?*

20*

1*

CI

1,384*

?*

151*

3*

KrioRus

N/A

N/A

52

7*

Oregon Cryonics

8*

N/A

6

5*

SA

N/A

N/A

N/A

3*

Trans Time

?

?

3

1?

*=simplification, see explanation

The Membership statistics reported above are for living Members only. Both Alcor and CI patients are Members (except for the ACS patients at CI). The American Cryonics Society (ACS) has an organizational policy against publishing the number of Members it has in its organization. As of April 2017 the 20 ACS patients were all in storage at the Cryonics Institute (CI). ACS has had one part-time clerk to do office work and has otherwise relied on volunteers. Alcor has 9 full-time staff, 1 consultant, and 1 regular volunteer. The 151 patients in storage at CI includes 20 ACS patients. KrioRus has no Membership program, and the method of counting patients is odd — a few are not stored by KrioRus. KrioRus has 4 full-time and 3 part-time employees as well as numerous volunteers.

CI is a subcontractor for storage of 20 ACS patients. CI has three paid staff (two full-time and one part-time), a few contractors and many volunteers. Accounting is done by CI Treasurer Pat Heller (a CPA) with auditing by another CI Director. Trans Time does not report its Membership numbers. Suspended Animation (SA) is a subcontractor which provides Standby/Stabilization/Transport (SST) only to other cryonics organizations (ACS, Alcor and CI), so it has no Members or Patients — so the reporting of Members or Patients for SA is "Not Applicable" (N/A). SA makes extensive use of subcontractors when needed.

Alcor and CI member numbers are not directly comparable because the word "Member" has different meanings for the two organizations. Membership in CI provides the privilege of obtaining cryopreservation services: pet, DNA or human cryopreservation. Many join CI only to store DNA or pets or to support CI, including some Alcor Members. Some Alcor Members have even made arrangements to use CI as a "back-up". Alcor does not allow its Members to have Alcor as a "back-up". Prior to April, 2012, all Alcor Members had made arrangements (ie, funding and contracts in place) for human cryopreservation and SST, but in April 2012 the Associate Alcor Member program was introduced. Associate Alcor Members do not have any cryopreservation arrangements with Alcor.

ForApril 2017, Alcor reported 1,639 living Members, 1,132 of whom had made arrangements for human cryopreservation, and 357 of whom were Associate Members. Of the 1,384 CI Members in April 2017, 212 of those had made arrangements for both human cryopreservation and standby/stabilization/transport (all with SA). In September 2015, CI ceased reporting how many of it Members have funding and contracts for cryopreservation. Historically, less than half of CI Members have been funded (prior CI statistics). Since 2006, CI offers a 'partnership' arrangement for CI Members for SA SST.

As noted in the previous section, Trans Time is currently storing patients, but (despite what their website says) is not currently seeking new Members or Patients.

In 2011 and 2012 SA reorganized its staff to have more part-time employees and contractors, and for much of 2012 and 2013 SA was re-organizing to have facilities in both California and Florida.

Oregon Cryonics has an owner (Jordan Sparks) and four other full-time employees. OC has 9 Members, but is no longer accepting new Members..

The term neuropreservation (or "neuro") generally refers to the practice of cryopreserving only the head rather than the whole body. A "neuro" is usually a whole head, not just the brain, but sometimes only the brain is cryopreserved. Keeping the whole head to preserve the brain is convenient for both perfusion and storage (the skull protects the brain). In some cases, however, "neuros" are brain-only. The following represent options various organizations say that they offer.

NAME

WHOLE BODY

NEURO

Alcor

Yes

Yes

ACS

Yes

No*

CI

Yes

No

KrioRus

Yes

Yes

Oregon Cryonics

No

Yes

SA

N/A

N/A

Trans Time

Yes

Yes

*=simplification, see explanation

Alcor states that its Members have the option of having their whole body cryopreserved or only their head ("neuro") — with different fees applicable to each choice. In April 2017, Alcor reported having 93 neuro, 54 whole body, and 4 neuro+whole bodypatients, whereas KrioRus reported 25 neuro and 27 whole-body patients. Trans Time has one whole body and two brains.

All CI Members with human cryopreservation arrangments are "whole body". ACS states that it does not have a policy against neuropreservation, but as long as it only uses CI as its subcontract or for storage it cannot offer neuro-cryopreservation as an option. Suspended Animation (SA) is a subcontractor which provides Standby/Stabilization/Transport only to other cryonics organizations, not storage, so the question of storage options with SA is "Not Applicable" (N/A).

Oregon Cryonics only stores heads and brains. As of February, 2016 Oregon Cryonics was chemically preserving three human brains, and cryopreserving one dog brain.

Cryopreservation and Yearly Fees

Comparing fees for human cryopreservation and yearly Membership or Emergency Responsibility is difficult to summarize in table form because the policies, procedures and options between the cryonics organization are so different. A great deal of explanation is required. Note that the high prices for human cryopreservation are generally covered by life insurance policies. The following represent the fees that the following organizations state that they charge.

NAME

WHOLE BODY

NEURO

YEARLY FEES

Alcor

$200,000*

$80,000*

$620*

ACS

$155,000*

N/A

$376*

CI

$28,000*

N/A

$120*

KrioRus

$36,000*

$12,000

None

Oregon Cryonics

N/A

$25,000*

None

SA

N/A

N/A

None

Trans Time

$150,000

$50,000

$96*

*=simplification,see explanation

To Alcor's yearly fee of $620 annual dues, those living in the United States and Canada must add $180 yearly SST fees for a total of $800 per year. A lifetime payment plan is also available. SST service is not available to Alcor Members outside of the US and Canada, but a $15,000 surcharge is added to whole body and neuro prices in the United Kingdom, and a $25,000 surcharge is added to the prices paid by those living in other countries. For details on Alcor pricing, see Schedule A: Required Costs and Suspension Funding Minimums.

The prices given for the American Cryonics Society (ACS) are intended to reflect comparable service to what Alcor provides. In fact, ACS has a very wide menu of options and prices available, including reference to a "California Procedure" which is intended to be distinguished from the"Michigan Procedure" offered by the Cryonics Institute. The yearly fee for an ACS Member is $376 for the first four years and $300 per year thereafter. For details on ACS options and fees, see:www.americancryonics.org.

The Cryonics Institute (CI) charges $28,000 for perfusion and storage of a Lifetime Member and $35,000 for a Yearly Member. These prices do not include funeral director costs or shipment to CI for non-local cases. (When CI was begun it was imagined that every state would have at least one cryonics service provider.) The Lifetime CI Member has paid a one-time $1,250 fee and the Yearly CI Member has paid a $75 initiation fee and is paying a $120 yearly fee. Discounts for additional family members and underage family members apply only to Lifetime Memberships. For service more comparable to what Alcor provides — including Standby/Stabilization/Transport (SST) — a Lifetime Member pays $88,000 and a Yearly Member pays $95,000. For details on CI pricing see Membership andDetails Concerning SA Standby and Transport for CI Members.

For $49,000 KrioRus states that it offers Russians (Europeans?) the option of shipment and storage at the Cryonics Institute in the USA.

Oregon Cryonics charges $25,000 to cryopreserve a whole head, $18,000 for a brain with braincase, and $14,000 for a brain without the braincase. Oregon Cryonics will chemically preserve a brain for as little as $1,000 (see Oregon Cryonics Service Fees for details).

As noted in previous sections, Trans Time is currently storing patients, but (despite what their website says) is not currently seeking new Members or Patients.

Suspended Animation (SA) is a subcontractor which provides SST only to other cryonics organizations, not Membership or storage, so the question of these options with SA is "Not Applicable" (N/A).

Human Cryopreservation Procedures

Human cryopreservation procedures are much too complex to be summarized effectively here.

Alcor's procedures are summarized on a page of the Alcor website called Alcor Procedures. But is it also very helpful to read actual case reports of Alcor patients in the Cryopreservation Case Reports section of the Alcor website library.

CI has a summary of its procedures on its website calledGuide to Cryonics Procedures. CI procedures do not include Standby/Stabilization/Transport (SST), though CI will advise Members on obtaining assistance through local funeral directors. CI Members residing in the continental United States who wish to obtain SST can do so by subcontracting with Suspended Animation, Inc. (SA).

Although the American Cryonics Society (ACS) has equipment and volunteers which could be used if necessary, ACS basically relies on SA for Standby/Transport and CI for Perfusion/Storage.The human cryopreservation procedures of Trans Time and KrioRus are not documented on their websites.

Funding Cryonics by Insurance
The cost of cryonics is many thousands of dollars, but most cryonicists cover these costs with life insurance policies that name a cryonics organization as beneficiary. Premiums of life insurance policies are most affordable for those who are young and healthy. It is not prudent to seek life insurance in old age or after a terminal illness (when life insurance may be unobtainable). Nor is it prudent to believe that cryonics arrangements can be made efficiently or successfully when in a terminal condition.

Rudi Hoffman sells the great majority of cryonics life insurance policies. It makes good sense to take advantage of Rudi's considerable expertise in matters of cryonics and life insurance. (A sincere and unpaid plug for Rudi.)

by @ CTVNews.ca - Top Stories - Public RSS

Mon Feb 12 08:56:00 PST 2018

U.S. President Donald Trump unveiled a US$4.4 trillion budget for next year that heralds an era of $1 trillion-plus federal deficits and -- unlike the plan he released last year -- never comes close to promising a balanced ledger even after 10 years.

by @ ImmInst Active Topics

Sun Feb 11 18:46:52 PST 2018

Hey,

For a few years now, I've been more or less regularly reading discussions, learning about a host of interesting topics and exploring all Longecity has to offer while never creating an account for some reason. Personally, I believe that this at least in part may have been rooted in the fact that, even though I might appear knowledgeable and am very interested in a number of topics at home on this site, I never truly felt as if I could add something so substantial that it would warrant me making an account and actively participating. I've now decided to do so anyway and, if we are lucky, I may actually be able to add something to this project.

In terms of interests, I am first and foremost fascinated by technology. Of any kind. The mechanics behind an automated watch are just as interesting to me as the inner working of a heater. A circuit board just as mesmerizing as a well engineered differential. You name it and I will want to understand it. This, being the case since my early childhood, though has lead me to realize that, what fascinates me the most isn't technology itself, as incredible as it is, but rather that we, as humans are able to accomplish so much with so little.

With other words, I've been struck with awe ever since I first looked into the human brain that many years ago. On average around 3lb heavy, is it the most complex thing in the as yet known universe. Despite its diminutive size though, we as a species owe everything to it. So what when, or rather if, there will be a day at which our brains have reached their limit?

The printing press was invented and popularized in the 15th century. It revolutionized the way information was accessible, the way information could be stored and the way information could be stored and the way information could be transferred. Now, not even 600 years later, a large chunk of the Earth's population has free and open access to most everything our species has accomplished. At any point in time and almost anywhere.

Technology is going to progress even further and, depending on whom you ask, may actually advance exponentially. We have been lucky so far that humans are very good at adapting to new scenarios. Though there will come a point, maybe in the not-so-distant future, or maybe 10000 years from now, that this won't be enough. That technology out-paces our monkey-brains. You may disagree, but I personally feel that this is more a question of when, rather than if.

Now, this line of thinking has led me, a few years ago, to consider whether or not it may be a good idea to at least entertain the thought, that science should look into the idea of "enhancing" the human brain. That lead me down a rabbit hole so deep, I'm still falling. The research being done is highly fascinating, so much so that I wrote a "pre-university paper" (part of the Austrian equivalent to the "A-Levels") looking into "Neuro Enhancement", its viability, the science behind it, dangers stemming from it, moral and ethical considerations, as well as much more.

I could get into it in length again, talking about key questions like "How would one measure "cognitive performance" and what does actually fall under that label?" among others. But I'll leave it at this for now.

Now, you may think that this has only a minimal relation to the actual focus of Longecity, as, on first sight, I appear to not really be focused on the main reason this site exists, considering and, perhaps someday, finding ways to make death a choice, rather than a necessity. But for me, this is a matter of perspective. My personal hypothesis, our monkey-brains are to "stupid" to ever find a proper way to immortality among other things, aside, I have a key believe.

Even if, some day, we find a way to stop our telomeres from shortening (or whatever you personally believe is the root cause of ageing), our brains, is my firm belief, are going to become older anyway. Thinking back, the way I was able to connect, understand and learn new information during my childhood is inherently different to what I am experiencing now. For the record, I am currently at the age believed by some to be the "ideal age" for a humans brain. Young enough to still be adaptable, yet already more or less "properly wired up". With other words, around 20. Yet I believe that there are some things that, as a child, I might had been able to more efficiently "learn". That for me, is something I feel we should always keep in mind when it comes to "proper anti-ageing", not just the body, but the mind need to be kept young.

My biggest fear is that there may come a day when I get to test whatever new amazing device the tech-giants release, yet I am unable to properly understand what I'm doing. I may be able to learn operation, I may be able to become proficient, but I may never again be able to explain why and how what I'm doing works.

If you are around my age, you may know this from your (grand-)parents. You might be able to show them how to properly operate their new smartphone, you may even get them to more or less get the hang of social networking, but still, the way they use these devices they never grew up with is inherently different from you. Even if you do not understand what happens in the background, you interact different with the tech you grew up with. That is something I am slightly terrified off.

Anyway, this introduction is already going on for quite a bit longer than almost anybody will care to read so thanks to those who actually managed it. You are either very patient or on Adderall, the latter I personally do not like from a neuroscientific level, as I do detest the "all-or-nothing" approach to Neuro Transmitters substances like it bring to the table. Same goes for Dopamine-Reuptake-Inhibitors and the lot.

By the way, I live in Austria, like salty stuff more than sweets, am somewhat of a Car guy, enjoy Games, as well as Anim(ation of all kind)e and movies, hope to try as much as I can in this lifetime, would kindly ask for criticism of any kind as I feel it is necessary to improve and apparently enjoy writing.

by undefined @ Canadian CattlemenCanadian Cattlemen

Wed Feb 07 12:29:21 PST 2018

I’ve received inquiries from cow/calf producers and backgrounders regarding the purchase of price insurance for feeder cattle. In early November the March futures made contract highs but since then have trended lower. At the same time, ther cash continues to trade near 52-week highs. It appears the Canadian feeder market has divorced from the feeder […] Read more

by @ LongeCity - Articles

Fri Jul 18 16:26:34 PDT 2014

Cryonics is a method of ‘medical time travel’ - placing the body in biostasis after legal death with the hope that future technology will be invented which can revive the body. To most people who share LongeCity’s mission cryonics is the ‘second worst thing’ that can happen to you, but nonetheless a viable alternative to burial or creation.

Cryonics prices vary (an overview can be found on this page maintained by Cryonics expert and LongeCity Advisor Ben Best) but it is affordable to nearly everyone via life insurance… nearly everyone. A few people who really want cryonics cannot get life insurance: After an accident, LongeCity Member James Swayze found himself quadriplegic and unable to get insurance. The life of LongeCity Member William O’Rights took a turn for the worst when he was diagnosed with aggressive throat cancer after having been suddenly deprived of all funds. Kim Suozzi was 23 and had not yet heard about cryonics when she was diagnosed with terminal brain cancer. Aaron Winborn heard of her case - and cryonics- only when the debilitating effects of Lou Gehrig's Disease had already begun to paralyse him. All these people were eventually offered a cryonics provision through the generous donations of others in our community.
We want to continue this proud tradition, looking out for those who share our common dream in unlimited lifespans, in the shadow of imminent death and despair.

However, this needs to be done carefully. It cannot be stressed enough that cryonics is affordable to most people if they only have the foresight to act early and arrange affordable life insurance. This element of personal responsibility is at the heart not just of cryonics. If we establish a hardship scheme, it must not create a moral hazard, and incentive to put things off as too unpleasant and complicated to think about until it is too late. Of course, we must also ward against fraud and abuse. An element of careful analysis and due diligence is therefore required, looking into the circumstances of each individual case.

The LongeCity cryonics hardship fund has two purposes:
1) To support a (volunteer based) infrastructure for maintaining the scheme and exercising the due diligence mentioned above
2) When a hardship case has been endorsed by LongeCity, we will use the hardship fund to help to fundraise for that individual by matching further donations. All these donations will go to a dedicated account for that person’s cryopreservation, never to the individual directly.

Applicants to our cryonics hardship fund must
- co-operate fully with LongeCity appointed auditors and reviewers
- genuinely be unable to not fully fund their cryosuspension and not have a reasonable chance of doing so prior to their likely death
- help to fundraise for their cause and help raise public awareness for cryonics

In the past, we have partnered with our friend in the Venturist community on cryonic hardship cases. We hoping to do so again on future occasions.

by @ Articles - Articles

Fri May 19 12:12:06 PDT 2017

Sven Bulterijs first discussed the potential utility of anti-diabetic substance metformin six years ago on LongeCity. Now Sven returns to the topic with a comprehensive and thoughtful discussion of the recent findings and further background information
⇒ read the article in "Sven's Science Corner" blog

by GIS @ Gastrointestinal Society

Mon Jun 26 09:00:07 PDT 2017

British Columbians will soon be invited to get good advice about their gut at Badgut.org, thanks to a generous airtime donation by the province’s broadcasters. The British Columbia Association of Broadcasters (BCAB) announced its members have chosen the GI (Gastrointestinal) Society and its associated registered charity, the Canadian Society of Intestinal Research, as this year’s [...]

by @ Articles

Fri May 19 12:12:06 PDT 2017

Sven Bulterijs first discussed the potential utility of anti-diabetic substance metformin six years ago on LongeCity. Now Sven returns to the topic with a comprehensive and thoughtful discussion of the recent findings and further background information
⇒ read the article in "Sven's Science Corner" blog

by @ LONGECITY Community Blog List

Fri Jun 09 02:08:00 PDT 2017

The forum structure at the heart of LongeCity works well in facilitating a free flow of communication and information exchange.Other more structured ways of curating information have their own advantages, but their adoption appears to be more difficult.

It took some time for the new feature to gain traction. In some areas this worked ok, in others we still don't have any entries.

To further promote the feature we are launching a small COMPETITION for theBEST REGIMEN in each category.

On Sept.1st LongeCity leadership will draw up a shortlist of the most promising entries for each existing category:

Life Extension, General Health;

Alertness, Cognition, Mood

Sports, Performance, Bodybuilding

Medical

Weight Loss

Beauty, Cosmetics, Skin, Anti-Aging

This shortlist will be based (but not necessarily bound) by the average of the "star ratings" an entry has received from all LongeCity readers! The Immortality Institute Members will then vote on a winner from each shortlistThe winner in each category* will receive $100 (via paypal) and ₮100.

(* yes, that means that the winning chance in the currently empty, or sparsely populated categories might be higher)

At least for the duration of the competition, the old 'stacks' forums will re-open. We hope that by now everyone has understood the distinction we are aiming for: the 'regimen' feature is for presenting and discussing structured regimens that can be considered, compared and potentially adopted by others down the ages, the forums are for more free-wheeling conversation that might be more speculative, protracted and less likely to hold a swift take-away message for others.

by undefined @ Canadian CattlemenCanadian Cattlemen

Mon Feb 05 12:41:02 PST 2018

Ontario cattlemen and the province have begun several programs to encourage more farmers to start raising beef in northern Ontario — where it is colder and the land is more suited to bush and cattle than corn and soybeans. Interest from producers considering a move north has been gaining momentum, and in mid-August 2017, the […] Read more

by Ken Silvers @ Probiotics Center

Fri Sep 01 03:18:27 PDT 2017

IBS treatment does not have to be expensive or complicated. In fact, some of the most effective ways to alleviate symptoms of IBS are either free or inexpensive. Here are five suggestions that can alleviate many gut problems. IBS treatment—5 simple tips 1. Probiotics IBS treatment includes alleviating symptoms of inflammation, bloating, constipation and pain. People […]

by Owen Alexander @ Alt Protein

Tue Jan 23 10:16:24 PST 2018

There are plenty of aggressively-marketed supplements out there that claim they improve your weight loss results as well as your overall health. However, we all know that not all of those products actually work and they don’t level up to the claims made by their marketing teams. If you are wondering which powder supplement might ... Read moreThe Blendfresh Whole Food Powder Review- Is it for you?

by @ Articles - Articles

Sun Aug 20 11:04:47 PDT 2017

When Darwin’s theory of evolution by natural selection was established, biologists were puzzled by the existence of senescence and aging among all organisms. Why did the evolutionary pressure not produce immortal species? They concluded that even the power of evolution has its limitations. It took almost hundred years to reach the idea that mortal individuals may be preferred by nature for following reasons — the genes resulting in advantage in early life might cause damage in late life, and the reproduction starts as soon as possible. Around the middle of twentieth century, there finally was a framework for the gerontological research conduced in the following decades — the first evolutionary theories of aging (Gavrilov & Gavrilova, 2002).
There are two major groups of theories aiming to explain the mechanism of aging, so-called programmed and error theories. The programmed ones are based on the senescence-causing nature of certain genes (these are also called evolutionary theories), hormones or the immune system. Error theories claim that we age because of general damage caused by cell weariness, metabolic rate, cross-linked proteins, free radicals or somatic DNA changes (Jin, 2010).
The beauty of various aging theories is that most of them are not mutually exclusive. We can see that newer theories do not necessarily oppose the old ones, but rather shed more light and offer more in-depth views on the process of senescence.
The pioneering idea from 1882 was Weismanns’s theory of programmed death (also called wear-and-tear theory) claiming something like apoptosis of the multicellular organism. Although disproved by experiments, his theoretical explanation of the mechanism predicted the discovery of Hayflick limit (Gavrilov & Gavrilova, 2002). According to Weismann’s first conception, nature priorities young individuals over elderly because of limited resources.
Pearl stated his ‘rate of living’ theory of aging in 1928, although the idea comes from Rubner who, in 1908, suggested that every organism has limited amount of metabolic energy and therefore its age depends on the rate of metabolism which correlates with organism’s size (Pearl, 1928). Most consider the rate of living theory to be flawed (Lints, 1989; de Magalhaes, Costa, & Church, 2007; Vaanholt, Daan, Schubert, & Visser, 2009).
A few decades later, the following evolutionary models have emerged:
Medawar’s hypothesis of mutation accumulation proposes that aging is a by-product of natural selection — genes causing senescence in later stadium of life cannot be eliminated because the genetic information was most likely already transferred to successors by individuals in their early adulthood (Gavrilov & Gavrilova, 2002). This theory from 1952 is considered the first modern theory of aging. Charlesworth confronted Medawar’s model with a discovery of late-life mortality plateaus and in 1994 presented so-called modified mutation accumulation theory (Charlesworth, 2001; Ljubuncic & Reznick, 2009).
In his antagonistic pleiotropy theory (also called ‘pay later’ theory), Williams in 1957 expressed the idea that even the same genes which cause trouble at advanced age may be advantageous in earlier stages of life, and therefore be not only tolerated, but even preferred by natural selection (Gavrilov & Gavrilova, 2002).
In 1979, Kirkwood extended this theory to the disposable soma theory — organisms may save energy by reducing accuracy in cells metabolism and invest it in faster development and reproduction (Kirkwood & Holliday, 1979). This is the last one of famous, genes-orientated evolutionary models.
The following can be classified as programmed theories:
The neuroendocrine theory proposed in 1954 by Dilman says that the main cause of aging is a loss of receptor sensitivity of the hypothalamus over time, and therefore its control of adequate production of hormones declines which leads to ineffectiveness and lower hormone levels in organism. It is an attempt to explain a high occurrence of degenerative diseases in late age (“Neuroendocrine Theory of Aging: Chapter 1,” 1999). Research on hormonal signaling pathways confirms that hormone levels have at least a partial role in determining longevity (van Heemst et al., 2005).
In 1964, Walford suggested his immunologic theory of aging — due to increasing diversity of cells, the immune system looses its efficiency with age which leads to insufficient responses against pathogens as well as to autoimmune reactions against self proteins (Walford, 1964).
All following attempts to explain the mechanism behind a process of aging are usually called error or damage theories.
Bjorksten’s "crosslinkage theory" says that proteins become linked together in presence of certain crosslinking agents, and after some time, accumulation of these molecular aggregates causes decline in tissue functions. This theory from 1942 is no longer popular (Bjorksten, 1968). Later research has showed that advanced glycation end products (AGEs) accumulate in collagen and lead to outcomes predicted by Bjorksten (Verzijl et al., 2002; Aronson, 2003).
These days very popular among researchers and public, the free radical theory was suggested by Harman in 1956. His idea was that the occurrence of free radicals, or reactive oxygen species naturally produced in living organisms, leads to macromolecular damage which accumulates and causes physiological changes known as senescence (Harman, 2009). Later he suggested the reactive oxygen species formation takes place mainly in mitochondria which causes a decline in important mitochondrial functions (Harman, 1972). Because of the theory’s popularity, various extensions of Harman’s model were created, usually considering different sites as a main target of free radicals.
Failla’s somatic mutation theory from 1958 posits that increasing number of mutations of genetic material causes a decrease in cellular, organ and body functions (Failla, 1958; Gensler & Bernstein, 1981; Kennedy, Loeb, & Herr, 2012). The theory received a lot of criticism in previous decades (Vijg, 2000). Kaya, Lobanov and Gladyshev (2015) investigated aging in yeast and failed to find evidence in support of Failla’s thesis.
Orgel proposed his error catastrophe theory in 1963. He saw the cause of aging in accumulation of malfunctioning proteins coming from errors during protein translation (Orgel, 1963). This theory never gained popularity and was soon disproved (Gershon & Gershon, 1976).
Alexander in 1967 extended Failla’s theory by hypothesizing that DNA damage instead of mutation is the cause of aging (Alexander, 1967). These days, this version called
"somatic DNA damage theory of aging" is more often used by scientists (Freitas & de Magalhaes, 2011; Soares et al., 2014). Evidence suggests that more damage happens in mitochondrial DNA than in nuclear DNA (Ames, 2009).
In 2002, Brunk and Terman published the mitochondrial-lysosomal axis theory. It states that defective macromolecules derived from mitochondria undergo further changes in lysosomes to become lipofuscin inclusions. These end products decrease cell’s autophagocytotic capacity which leads to more mitochondrial defects (Brunk & Terman, 2002).
Zs.-Nagy’s "membrane hypothesis" focuses on a decline of mitochondrial functions due to lessened membrane permeability caused by residual heat coming from nerve signals as well as by reactive oxygen species (Zs.-Nagy, 2014).
Recent versions of damage theories claim that free radicals are only one kind of senescence-causing by products of metabolism but the real initiator of all the inevitable damage is biological imperfectness. In other words, there are always types of damage which lack adequate repair mechanisms in organism and the most severe source of errors depends on actual conditions (Gladyshev, 2013; Gladyshev, 2014). This idea comes from the
"reliability theory", which focuses on systems failure in machines (Gavrilov & Gavrilova, 2001).
In spite of many research programs and lots of scientists involved, the unifying factor in aging is at the moment still unknown.

References

Alexander, P. (1967). The role of DNA lesions in the processes leading to ageing in mice. Symp Soc Exp Biol, 21, 29-50.

Orgel, L. (1963). The Maintenance of the Accuracy of Protein Synthesis and its Relevance to Ageing. Proceedings Of The National Academy Of Sciences, 49(4), 517-521.
http://dx.doi.org/10.1073/pnas.49.4.517

by medium bad @ Alivebynature – Evidence Based Reviews

Mon Feb 12 10:05:10 PST 2018

The results achieved by Professor David Andrew Sinclair in his quest for reversing aging have moved from the exceptional to the phenomenal. This brief essay lists the evidence and suggests what may be the best value for money route to implementing an effective lowest-cost protocol for delivering similar or the same results. This brief Answer/Essay […]

by Ken Silvers @ Probiotics Center

Tue Jun 27 13:26:45 PDT 2017

Benefits of probiotics are available for everyone with a stomach. And probiotics are essential in case of a poor gut and chronic disease. Probiotics are called friendly bacteria and indeed your body needs many friends. In fact, billions to stay well! The aim of this article is to provide vital information on how men, women […]

Product Review Many individuals take probiotics to reduce symptoms from gastrointestinal (GI) disorders or to improve their overall intestinal health. Since most people view probiotics as safe, natural, and effective, they are popular products. However, not all probiotics are equal. The World Health Organization defines probiotics as “live microorganisms which when administered in adequate amounts …

by @ LongeCityNews

Mon Feb 12 03:09:52 PST 2018

Rising numbers of senescent cells are one of the root causes of aging, a process that arises from the normal operation of youthful metabolism, yet results in accumulated damage and failure over time. Senescent cells generate signaling that degrades tissue function, breaks down and remodels tissue structure, spurs chronic inflammation, and alters the behavior of surrounding cells for the worse. Evidence shows their presence to be a contributing cause of a range of common fatal age-related conditions. In a youthful body, near all cells that become senescent and fail to self-destruct as a result are promptly eliminated by the immune system. In an aged body, the immune system is worn and degraded; as a consequence many more senescent cells survive to linger. We are machines of interacting, dependent parts. Damage and failure in one component speeds the onset of damage and decline in others. The age-related failure of the immune system is an important part of the acceleration of functional decline in later life.

Whilst there is currently little understanding concerning the mechanisms governing macrophage mediated recognition of senescent cells, the processes are probably not specific to senescent cells. Rather, the more characterised molecular mechanisms associated with macrophage recognition during cancer immunosurveillance and apoptotic cell clearance may also be pertinent for senescence surveillance. Apoptotic cells have been shown to preferentially express specific cell surface antigens which can be recognised by naturally occurring antibodies (IgMs) that enable phagocytosis by macrophages. As such, it can be speculated that senescent cells may also express specific cell surface antigens which would not only provide insights into the mechanisms mediating immune clearance, but would also provide a means to specifically identify senescent cells in tissues.

Surface expression of CD47 acts as a "don't eat me" signal, sending inhibitory signals through SIRPα, a receptor expressed on the surface of macrophage, ensuring that healthy cells are not inappropriately phagocytosed. Therefore, the downregulation of CD47 would be required for macrophages to target damaged "self" cells. One study has demonstrated that induction of tumour cell senescence via c-Myc inactivation leads to the downregulation of CD47 which consequently promoted tumour regression. Whether CD47 downregulation in this instance is a specific response to c-Myc inactivation or activation of the senescence program is unclear. It would make biological sense to downregulate CD47 during cell senescence to enable removal of damaged "self" cells, but further research is required.

Immunotherapeutic strategies already in development for combating cancer may one day be repurposed for targeting senescent cells for the alleviation of age-related diseases. In addition, identifying further molecular changes associated with senescent cells, especially cell-type specific alterations, would be advantageous for developing therapeutic approaches for targeting senescent cells. Since senescent cells can also be beneficial in the short term, the elimination of acute senescent cells could be problematic. Therefore, the identification of therapeutic targets specific to chronic senescence which are absent in acute senescent cells would be highly desirable.

One of the mechanisms by which natural killer (NK) cells specifically recognise and kill senescent cells is via the surface expression of NKG2Dligands. Since many tumour cells also express NKG2D ligands, such ligands have been suggested to be a useful target for immunotherapeutic approaches in cancer, and so could be adapted for senescent cell clearance. For example, the use of engineered immune cells such as chimeric antigen receptor (CAR)T cells to target specific molecules on cancer cells has great potential as an anti-cancer therapy. As such, it may be possible to target senescent cells by engineering T cells to express a NKG2D CAR which recognise NKG2D ligands on the surface of senescent cells.

An adaption of cancer vaccines could also be considered for boosting immune clearance of senescent cells. Although a universal biomarker of cell senescence has not been identified, the exposure of senescent cell membranes to immune cells may evoke an immune response to antigens not yet identified. In one approach, senescence vaccines would involve the isolation of senescence specific antigens (SSAs) which are then exposed to dendritic cells, professional antigen presenting cells. In response to SSA uptake, dendritic cells process and express these antigens on their cell surface which can then be recognised by T cells. T cell interaction with these antigens promotes T cell activation, differentiation, and ultimately killing of target cells.

by @ Articles - Articles

Sat Sep 09 06:57:38 PDT 2017

The word "nootropic" derives from the Greek words nous, or "mind", and
trepein meaning "to bend or turn". It was first coined by Romanian psychologist and chemist, Corneliu E. Giurgea after synthesizing
Piracetam.
For Giurgea a nootropic drug should have the following characteristics:
1. They should enhance learning and memory.
2. They should enhance the resistance of learned behaviors/memories to conditions which tend to disrupt them (e.g. electroconvulsive shock, hypoxia).
3. They should protect the brain against various physical or chemical injuries (e.g. barbiturates, scopalamine).
4. They should increase the efficacy of the tonic cortical/subcortical control mechanisms.
5. They should lack the usual pharmacology of other psychotropic drugs (e.g. sedation, motor stimulation) and possess very few side effects and extremely low toxicity.

In fact, most drugs commonly labelled as nootropics do not fulfill all of these requirements. Some of the best known (e.g. Adderall, Modafinil) seem to not fulfill any, as discussed later. Instead, other characteristics like (reputed increased alertness, focus or motivation) seem to be key to their popularity.
Because of deviating definitions nootropics are more broadly defined (e.g. in wikipedia) as drugs, supplements, or other substances that improve cognitive function, particularly executive functions, memory, creativity, or motivation, in healthy individuals.

Some nootropics from the very common to the :

Caffeine
Caffeine is the world’s most widely used stimulant (Nawrot, et al., 2003). It is used by over 90 % of North Americans every day (Mednick et al., 2008). It is widely used because of its positive effects on mood and alertness (Lorist & Tops, 2003)and vigilance and attention (Lieberman et al., 1987). However, these effects do not seem applicable / transferable to motor learning and verbal memory and are unable to reverse effects of sleep deprivation, with a dose of 200mg in low to moderate users (< than 2 cups a day) (Mednick et al., 2008). It is also shown to be ineffective in higher cognitive tasks involving working memory (Battig et al., 1984). Overall conclusions regarding the relation of caffeine and memory have been mixed. Positive effects might stem from caffeine withdrawal in high dosage users (Mednick et al., 2008).

Nicotine
With about 1,1 billion smokers worldwide in the year 2015 (WHO 2015) nicotine takes second place as the most widely used stimulant. It was shown that the application of nicotine in non-smoking males enhances performance in continuous performance tasks and therefore is said to improve attention and working-memory (Kumari, et al., 2003), which is in line with other studies suggesting that nicotine affects short-term memory in delayed free recall tasks (Sarah & Fox, 1998)
Another study examined nicotine’s effects on alertness and performance on a covert orienting task were measured. While nicotine decreased overall reaction times in the covert orienting task, there was no change in the validity effect, the reaction time difference between validly and invalidly cued targets. However, nicotine significantly improved both EEG and self-rated measures of alertness. Nicotine seems to increases alertness in non-smokers, with no improvement in spatial attention using a covert orienting task (Griesar et al., 2002). Furthermore Nicotine seems to reduce distraction under low perceptual load by acting as a stimulus filter that prevents irrelevant stimuli entering awareness (Behler et al., 2015).

Methylphenidate/ Ritalin
Most college students I know will immediately think of Ritalin or Modafinil if they are asked to name a cognitive enhancer. Studies have found that 4.1% to 10.8% of college students in the US reported using prescription stimulants non-medically during the past year (Garnier-Dykstra, et al., 2012).
Methylphenidate (MPH - common brand name ‘Ritalin’) is used in treatment of attention deficit hyperactivity disorder (ADHD) and narcolepsy. Most studies focused on the its effects on Attention, Mood, Memory and executive functions. A single dose of MPH showed a positive effect on memory. Repeated doses of MPH had a mood elevating effect but also enhanced anxiety. No statistically significant effect was found in the outcomes attention, mood and executive functions. MPH had no significant effect on sleep-deprived individuals (Repantis et al., 2010). In a 2015 review the authors found some ‘publication bias’, relating to long-term and working memory and conclude that the effect in healthy subject is probably modest overall and that healthy users resort to stimulants to enhance their energy and motivation more than their cognition (Ilieva et al., 2015).

Modafinil
Modafinil is used in treatment of disorders such as narcolepsy, shift work sleep disorder, and excessive daytime sleepiness associated with obstructive sleep apnea. Most studies focused on its effects on attention, mood, memory, wakefulness and executive functions and motivation. A single dose showed positive effects on attention only. On sleep deprived individuals it was shown to have an impact on executive functions, on memory and wakefulness but there was an insignificant effect on mood and attention (Repantis et al., 2010). A 2012 meta-analysis found that Modafinil was likely effective but criticised the gaps in the literature. (Kelley et al., 2012)
A recent study on chess players found significantly enhanced performance with Modafinil or Ritalin but only when the players were not under time pressure (Franke et al. 2017).

Adderall
Mixed Amphetamine Salts also known under the brand Name Adderall became increasingly popular in recent years as an athletic performance enhancer and cognitive enhancer. Like Ritalin, it is also used to treat ADHD and narcolepsy.
Overall effects of Adderall on cognition have been reviewed as very modest, while having a huge effect on perception. It was found to enhance performance in word recall, embedded figures and Raven's Progressive Matrices, but only for lower performing individuals (Ilieva et al., 2013). Adderall might also impair creativity in high performing individuals (Farah et al., 2009).

L-theanine & Caffeine
L- theanine is primarily found in plants (e.g. in the leaves of green and black tea) and fungus. Results evidently demonstrated that L-theanine clearly has a pronounced effect on attention performance and reaction time response in normal healthy subjects susceptible to having high anxiety (Higashiyama et al., 2011).
A dose of L-theanine equivalent to eight cups of black tea improves cognitive and neurophysiological measures of selective attention, to a degree that is comparable with that of caffeine. The combination of Theanine and caffeine seem to have additive effects on attention in high doses (Kahathuduwa et al.,2016).
Studies suggest that 97 mg of L-theanine in combination with 40 mg of caffeine helps to focus attention during a demanding cognitive task (Giesbrecht 2010).

Bacopa Monnieri
Bacopa Monnieri is an herb which has been used in Ayurvedic medicine for centuries. Bacopa's primary mechanism of action is still unclear, it seems to be an anti-oxidant, a weak acetylcholinesterase inhibitor and a cerebral blood flow activator (Aguiar & Borowski , 2013).
There is some evidence to suggest that Bacopa Monnieri improves memory with little evidence of enhancement in any other cognitive domains (Pase et al., 2012).

Piracetam
Closing the circle to the beginning of this short introduction to the topic: Giurgea
first coined the term "nootropic" when he synthesized Piracetam in 1964. Since it is not approved by the US FDA, it is primarily used in Europe, Asia, and South America. It is commonly prescribed for cognitive impairment and dementia in several countries of Europe. Research suggests that Piracetam might also have a positive effect on healthy individuals. Subjects were given 3×4 capsules at 400 mg per day, in a double blind study. Each subject learned series of words presented as stimuli upon a memory drum. No effects were observed after 7 days but after 14 days verbal learning had significantly increased (Dimond & Brouwers, 1976).
It might also be beneficial for cognitive decline associated with age. Aging subjects did significantly better in a computerized perceptual-motor tasks when on piracetam than on a placebo. (Mindus et al. 1976).
While these old studies may not be that reliable, it is still held that
Piracetam's “efficacy is documented in cognitive disorders and dementia, vertigo, cortical myoclonus, dyslexia, and sickle cell anemia. While high doses are sometimes necessary, piracetam is well tolerated” (Winblad, 2005).
Since Piracetam was first synthesized many structurally similar compounds have emerged. These so called Racetams have poorly understood mechanisms of action; however, piracetam and aniracetam are known to act as positive allosteric modulators of AMPA receptors and appear to modulate cholinergic systems (Gualtieri et al., 2002).

This article is solely for information purposes, not a substitute for professional medical or dietary advice.
The provisos of the LongeCity user agreement apply.write
for LongeCity

by Owen Alexander @ Alt Protein

Tue Jan 23 19:57:31 PST 2018

Nowadays, greens powder supplements are flooding the fitness and nutrition market. Many of these brands claim to work amazingly and intentionally exaggerate their products’ properties without providing evidence or ways to measure those claims. All these aspects are not an issue when it comes to ORAC Energy Greens manufactured by the Paradise Herbs & Essentials ... Read moreThe Paradise ORAC Energy Greens Review You’ll Really Love

by @ LongeCity - Articles

Article 1The following shall be the letter of the agreement that all visitors, Members and their guests will be asked to abide by when interacting with the
LongeCity/ Imminst ("LongeCity") website Please read this Agreement carefully before accessing the Site.

Section03 Content (a) LongeCity provides an open platform for registered users to share text, video, audio, programmes, scripts, files, hyperlinks and other material on the Site ("Content") as long as such sharing is lawful and not in contravention of this Agreement. However, LongeCity does not undertake to scrutinise, evaluate, test or verify any Content prior to it being shared on the Site.(b) Content from the Site may be downloaded solely for your own non-commercial use.(c) You understand that by using the Site, you may be exposed to Content that you may deem offensive, indecent or objectionable.(d)
LongeCity does not control the Content contributed by users and, consequently, provides no guarantee as to the correctness, integrity or fitness of such Content.(e) Content are the responsibility of the person from whom such Content originated. You agree that you and not LongeCity, are entirely responsible for all Content that you upload, post, email, link, transmit or otherwise make available via the Site.(f) When contributing Content, you agree that this Content may be edited or deleted or rendered to display in a different manner at the discretion of
LongeCity.(g) LongeCity will not use Content you contribute for commercial gain without your express permission, but cannot warrant or guarantee in any way that others who you decide to share the Content with might not use it for commercial activities.
(h)LongeCity cannot be held responsible for any Content that has been contributed through its open platform. LongeCity will not react to requests to verify, redact, edit, delete or obfuscate any Content.

Section05 Limitation of Liability (a) In no event will LongeCity
be liable for consequential or incidental damageswhich may arise in connection with your use of the Site. Accordingly, you agree that
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by undefined @ Canadian CattlemenCanadian Cattlemen

Thu Feb 19 10:32:36 PST 2015

How do plants grow? This might seem like a pretty simple and harmless question, but Jean Baptista Van Helmont was curious about this so he did a pretty basic experiment to find out. The downside to his experiment was that he was arrested for it! Here is what he did in his own words: “I […] Read more

by undefined @ Canadian CattlemenCanadian Cattlemen

Tue Jan 02 13:09:21 PST 2018

I am a big fan of speakers at conferences that tell you about all the stuff that went wrong. I would rather learn from someone else’s mistakes than my own. I already have far too many “learning experience’s” here at Greener Pastures Ranching. Too many of the speakers explain how easy and trouble-free their particular […] Read more

Probiotics, defined as ‘live microorganisms, which when administered in adequate amounts, confer a health benefit on the host’, are finally becoming an option for gastroenterologists in Canada, after being available for many years in Japan, ...

by GIS @ Gastrointestinal Society

Thu Apr 13 12:11:27 PDT 2017

The Gastrointestinal Society is thrilled to announce that it will be participating in the 2017 Scotiabank Charity Challenge! The Vancouver races will be happening on June 25, 2017, and the GI Society needs YOUR help to raise funds and awareness for those living with gastrointestinal and liver conditions across Canada. Runners can participate in either [...]

by @ LongeCityNews

Mon Feb 12 16:27:32 PST 2018

Comparatively little work on combinations of therapies takes place in the research community. I suspect this to be a matter of regulatory incentives. For example there is little room for commercial entities to be able to make money by combining established treatments owned by other entities. Similarly for researchers, the world of possible approaches is balkanized by intellectual property, while the disposition of the majority of research funding is ultimately guided by the promise of a pot of gold at the end of the road. That pot of gold is much harder to obtain when someone else owns the therapies involved, and all that is being done is to apply them together. The edifice of intellectual property is a great evil, and this is one of many reasons why that is the case.

Given this long-standing state of affairs, there is at present little data to guide our expectations on the bounds of the possible when it comes to combining large numbers of therapies in search of additive and synergistic effects. Some people think that we should forge ahead in the matter of slowing aging: take every intervention with good evidence to date, and run large numbers of them in the same mice to see what happens. Should we believe that various ways of manipulating the operation of cellular metabolism demonstrated to achieve 5-10% life extension in mice can combine to double life span in that species? Intuition suggests not, but I don't think it to be completely out the question. Nor is it unreasonable to try it and see, given a rigorous approach to experimental design. Sadly, no established funding institution would go for this; it would have to be funded through philanthropy.

Why do I think that this is unlikely to produce large enough results to make it worthwhile? Because the evidence to date strongly suggests that the scores of methods of manipulating metabolism to modestly slow aging are operating on just a few core processes, such as autophagy. These are the stress responses that produce the lengthening of life observed in calorie restriction, and we know that these mechanisms don't produce anywhere near the same degree of life extension in humans as they do in short-lived species. Everything is connected to everything else in cellular biochemistry. A given interaction between two proteins can be influenced by adjusting levels of any number of other proteins, with widely varying degrees of effectiveness and side-effects. So most methods of slowing aging are different views into the same method of action. The few combinations of approaches tried to date, involving only two methods, have resulted in mixed outcomes. Calorie restriction and mTOR inhibition may be additive, while growth hormone receptor knockout and mTOR inhibition interfere with one another, for example. That gives little insight as to the rest. It is hard to predict other results, beyond noting that a majority of interventions do appear to function through enhanced autophagy, and thus we might expect them not to combine in an additive way to any great degree.

What of the SENS rejuvenation biotechnology approach to aging, in which independent fundamental forms of cell and tissue damage are repaired? How will repair therapies combine? In this case we should expect additive effects: removing damage should be beneficial in proportion to the amount removed, at least when considered from a fundamental, reliability theory perspective. The mortality risk and longevity of a complex system of many redundant parts is dependent on its current load of damage. At this point we have no idea as to how that will turn out in practice, however. The contributions of different forms of damage may be significantly larger or smaller than one another. The results of two independent root cause forms of damage are not themselves independent: they interact, and probably significantly. Functional decline in one system spurs greater damage and functional decline in others, which is why age-related degeneration accelerates greatly in later life. It is a complex business. It isn't unreasonable to think that in some circumstances the results of rejuvenation therapies A and B will be indistinguishable from A alone, or that B will never achieve a great deal without being combined with C.

Can we envisage a world in which repairing cellular senescence alone produces no extension to life span because other, largely independent chains of damage and consequence are still life-limiting for old humans? That is becoming increasingly hard given the evidence to date for reversal of numerous age-related diseases to result from removal of senescent cells, not to mention the PAI-1 mutants who exhibit increased life span - but we know far more about senescent cell clearance than we do about any of the other SENS strategies. No-one is in a position to do more than make educated guesses about the results of combining senescent cell destruction with removal of mitochondrial DNA damage, or with clearance of specific lysosomal aggregates. Beyond "two should be better than one, but perhaps not in some specific cases" everything else will remain a mystery until the biotechnology is ready and the work is carried out. Making predictions seems a fool's game, given the degree to which the people closest to senescent cell research have been surprised by the scope and size of benefits observed in mice over the past few years.

by @ Articles - Articles

Tue Jul 18 14:03:16 PDT 2017

Sven Bulterijs continues his discussion of prominent compounds with potential life extension efficacy by looking not just at rapamycin but also at its target, the mTOR pathway, which has likely a key role in mediating lifespan.
⇒ read the article in "Sven's Science Corner" blog

by @ ImmInst Active Topics

Mon Feb 05 18:57:19 PST 2018

I'm looking for a source for Picamilon that is obtainable from the US.

I don't use this recreationally. Basically I'm using it as a rescue dose for extreme anxiety that is the result of protracted withdrawal from years of prescription z-drug use. Apparently my gaba receptors have not yet normalized 30 months after quitting nightly use of eszopiclone.

When I really get into a high anxiety state it's the only thing that will reliably pull me out of it that I feel isn't a massive threat to undoing whatever recovery I'm managed to build. I'm really trying to stay away from GABA receptor PAMs and don't believe that GABA itself will be as down regulating to these receptors.

I use maybe 150mg every week or so. I've got a bottle from 2015 that will be depleted in another month or two.

So does anyone know a reliable source that can get this material into the US in spite of our idiotic laws?

by @ LONGECITY Community Blog List

Wed Jul 26 05:52:30 PDT 2017

So, I was reading this over at the FDA and it dawned on me that these safety side effects were only likely to occur in people who are aged. In young people, it would very likely not be an issue. So here's the bigger issue:

If you take these away from young people or dissuade them from using them altogether, the young people will lose the opportunity to be healthy. Could it be policies like these that are fattening up America while Japan enjoys the slimmest healthiest lifestyle the world over?

Instead, I propose that we put age limits on supplements like these. We have minimum ages for alcohol and tobacco, so why not require carding for maximum ages and put in place a system to allow regulatory authorities to print a max age code on retail boxes and bottles. This of course leaves the looming problem of agism still at play and these regulations may negatively impact those who grow younger, but we can cross that bridge when we get there. For now, we just need to ensure that young people don't get fat and that those who are unfortunate enough to be fat when young can get to their optimum weight and experience that while they are still young.

As a nutritionist (and one who frequently recommends probiotics), I get a lot of questions about probiotics. Here I have compiled the most frequently asked questions and offered you my answers to help guide you in making good bacteria a part of your health routine.

by GIS @ Gastrointestinal Society

Wed Jan 17 10:09:47 PST 2018

The GI Society represents Canadians living with gastrointestinal diseases and disorders, including those who have experienced Clostridium difficile infection (CDI), and the devastating digestive symptoms that occur from this infection. We offer patient education on a wide array of GI conditions, in text and video formats, including a video on the development, symptoms, and treatments [...]

by @ Articles

Fri Jul 18 16:26:34 PDT 2014

Cryonics is a method of ‘medical time travel’ - placing the body in biostasis after legal death with the hope that future technology will be invented which can revive the body. To most people who share LongeCity’s mission cryonics is the ‘second worst thing’ that can happen to you, but nonetheless a viable alternative to burial or creation.

Cryonics prices vary (an overview can be found on this page maintained by Cryonics expert and LongeCity Advisor Ben Best) but it is affordable to nearly everyone via life insurance… nearly everyone. A few people who really want cryonics cannot get life insurance: After an accident, LongeCity Member James Swayze found himself quadriplegic and unable to get insurance. The life of LongeCity Member William O’Rights took a turn for the worst when he was diagnosed with aggressive throat cancer after having been suddenly deprived of all funds. Kim Suozzi was 23 and had not yet heard about cryonics when she was diagnosed with terminal brain cancer. Aaron Winborn heard of her case - and cryonics- only when the debilitating effects of Lou Gehrig's Disease had already begun to paralyse him. All these people were eventually offered a cryonics provision through the generous donations of others in our community.
We want to continue this proud tradition, looking out for those who share our common dream in unlimited lifespans, in the shadow of imminent death and despair.

However, this needs to be done carefully. It cannot be stressed enough that cryonics is affordable to most people if they only have the foresight to act early and arrange affordable life insurance. This element of personal responsibility is at the heart not just of cryonics. If we establish a hardship scheme, it must not create a moral hazard, and incentive to put things off as too unpleasant and complicated to think about until it is too late. Of course, we must also ward against fraud and abuse. An element of careful analysis and due diligence is therefore required, looking into the circumstances of each individual case.

The LongeCity cryonics hardship fund has two purposes:
1) To support a (volunteer based) infrastructure for maintaining the scheme and exercising the due diligence mentioned above
2) When a hardship case has been endorsed by LongeCity, we will use the hardship fund to help to fundraise for that individual by matching further donations. All these donations will go to a dedicated account for that person’s cryopreservation, never to the individual directly.

Applicants to our cryonics hardship fund must
- co-operate fully with LongeCity appointed auditors and reviewers
- genuinely be unable to not fully fund their cryosuspension and not have a reasonable chance of doing so prior to their likely death
- help to fundraise for their cause and help raise public awareness for cryonics

In the past, we have partnered with our friend in the Venturist community on cryonic hardship cases. We hoping to do so again on future occasions.

by @ CTVNews.ca - Top Stories - Public RSS

Mon Feb 12 17:46:46 PST 2018

U.S. President Donald Trump says Canada “does not treat us right,” an angry mother says her daughter’s 10-hour emergency room wait is unacceptable, and servers at an Ontario restaurant are speaking out against their boss’s “tip out” demand.

by undefined @ Canadian CattlemenCanadian Cattlemen

Fri Feb 09 10:38:04 PST 2018

There are several factors that play a role in cow fertility and some of them are interrelated. Whether or not a heifer will breed quickly (reaching puberty at a young age) or a cow will breed back in a timely fashion after calving and become pregnant will depend on a combination of genetics, nutrition, health, […] Read more

by @ LONGECITY Community Blog List

Thu Nov 16 10:12:00 PST 2017

I've been using a bunch of supplements and improvised materials that just haven't been done yet and have been getting great results. Then two nights ago I add a half dose of an adjuvant to my existing regimen that can slowly remove glucosepane, or so it seems. I have it on good authority that this mechanism will be effective. The new ingredient is working wonders. After I shaved this morning, my face felt smoother than it had in years (I change my blades very infrequently, this one is at least a few months old and the disposable battery is about a month). The over all appearance of my skin has improved greatly in the last few weeks. At this point it looks like a pointalism painter painted some younger spots on my skin in layers and the layering is continuing. Interestingly enough, I was out walking about in the sun and overcast skies at a nearby college for several hours yesterday and was expecting my skin to look worse. I do take 4 supplements to minimize the effect of the sun on my skin as I have a somewhat mild (in cosmetic terms... medically it's atypical, basically I have a high enough adrenaline response to deal with the inflammation rapidly and systemically so I feel the effects differently and only get a few zits and a spell of anxiety) case of polymorphic light eruptions or what I refer to as sun sensitivity. The supplements virtually ameliorate the sensitivity most of the time.

Anyways, my skin got much better, though it was perhaps a little red and more wrinkled in areas such as that between my thumbs and pointer fingers, and I was exhausted by the end of the day. The skin returned to normal when the inflammation subsided.

I feel like we're getting real close for those of us who are informed enough to start defeating aging on our own.

by @ Articles

Sat Sep 09 06:57:38 PDT 2017

The word "nootropic" derives from the Greek words nous, or "mind", and
trepein meaning "to bend or turn". It was first coined by Romanian psychologist and chemist, Corneliu E. Giurgea after synthesizing
Piracetam.
For Giurgea a nootropic drug should have the following characteristics:
1. They should enhance learning and memory.
2. They should enhance the resistance of learned behaviors/memories to conditions which tend to disrupt them (e.g. electroconvulsive shock, hypoxia).
3. They should protect the brain against various physical or chemical injuries (e.g. barbiturates, scopalamine).
4. They should increase the efficacy of the tonic cortical/subcortical control mechanisms.
5. They should lack the usual pharmacology of other psychotropic drugs (e.g. sedation, motor stimulation) and possess very few side effects and extremely low toxicity.

In fact, most drugs commonly labelled as nootropics do not fulfill all of these requirements. Some of the best known (e.g. Adderall, Modafinil) seem to not fulfill any, as discussed later. Instead, other characteristics like (reputed increased alertness, focus or motivation) seem to be key to their popularity.
Because of deviating definitions nootropics are more broadly defined (e.g. in wikipedia) as drugs, supplements, or other substances that improve cognitive function, particularly executive functions, memory, creativity, or motivation, in healthy individuals.

Some nootropics from the very common to the :

Caffeine
Caffeine is the world’s most widely used stimulant (Nawrot, et al., 2003). It is used by over 90 % of North Americans every day (Mednick et al., 2008). It is widely used because of its positive effects on mood and alertness (Lorist & Tops, 2003)and vigilance and attention (Lieberman et al., 1987). However, these effects do not seem applicable / transferable to motor learning and verbal memory and are unable to reverse effects of sleep deprivation, with a dose of 200mg in low to moderate users (< than 2 cups a day) (Mednick et al., 2008). It is also shown to be ineffective in higher cognitive tasks involving working memory (Battig et al., 1984). Overall conclusions regarding the relation of caffeine and memory have been mixed. Positive effects might stem from caffeine withdrawal in high dosage users (Mednick et al., 2008).

Nicotine
With about 1,1 billion smokers worldwide in the year 2015 (WHO 2015) nicotine takes second place as the most widely used stimulant. It was shown that the application of nicotine in non-smoking males enhances performance in continuous performance tasks and therefore is said to improve attention and working-memory (Kumari, et al., 2003), which is in line with other studies suggesting that nicotine affects short-term memory in delayed free recall tasks (Sarah & Fox, 1998)
Another study examined nicotine’s effects on alertness and performance on a covert orienting task were measured. While nicotine decreased overall reaction times in the covert orienting task, there was no change in the validity effect, the reaction time difference between validly and invalidly cued targets. However, nicotine significantly improved both EEG and self-rated measures of alertness. Nicotine seems to increases alertness in non-smokers, with no improvement in spatial attention using a covert orienting task (Griesar et al., 2002). Furthermore Nicotine seems to reduce distraction under low perceptual load by acting as a stimulus filter that prevents irrelevant stimuli entering awareness (Behler et al., 2015).

Methylphenidate/ Ritalin
Most college students I know will immediately think of Ritalin or Modafinil if they are asked to name a cognitive enhancer. Studies have found that 4.1% to 10.8% of college students in the US reported using prescription stimulants non-medically during the past year (Garnier-Dykstra, et al., 2012).
Methylphenidate (MPH - common brand name ‘Ritalin’) is used in treatment of attention deficit hyperactivity disorder (ADHD) and narcolepsy. Most studies focused on the its effects on Attention, Mood, Memory and executive functions. A single dose of MPH showed a positive effect on memory. Repeated doses of MPH had a mood elevating effect but also enhanced anxiety. No statistically significant effect was found in the outcomes attention, mood and executive functions. MPH had no significant effect on sleep-deprived individuals (Repantis et al., 2010). In a 2015 review the authors found some ‘publication bias’, relating to long-term and working memory and conclude that the effect in healthy subject is probably modest overall and that healthy users resort to stimulants to enhance their energy and motivation more than their cognition (Ilieva et al., 2015).

Modafinil
Modafinil is used in treatment of disorders such as narcolepsy, shift work sleep disorder, and excessive daytime sleepiness associated with obstructive sleep apnea. Most studies focused on its effects on attention, mood, memory, wakefulness and executive functions and motivation. A single dose showed positive effects on attention only. On sleep deprived individuals it was shown to have an impact on executive functions, on memory and wakefulness but there was an insignificant effect on mood and attention (Repantis et al., 2010). A 2012 meta-analysis found that Modafinil was likely effective but criticised the gaps in the literature. (Kelley et al., 2012)
A recent study on chess players found significantly enhanced performance with Modafinil or Ritalin but only when the players were not under time pressure (Franke et al. 2017).

Adderall
Mixed Amphetamine Salts also known under the brand Name Adderall became increasingly popular in recent years as an athletic performance enhancer and cognitive enhancer. Like Ritalin, it is also used to treat ADHD and narcolepsy.
Overall effects of Adderall on cognition have been reviewed as very modest, while having a huge effect on perception. It was found to enhance performance in word recall, embedded figures and Raven's Progressive Matrices, but only for lower performing individuals (Ilieva et al., 2013). Adderall might also impair creativity in high performing individuals (Farah et al., 2009).

L-theanine & Caffeine
L- theanine is primarily found in plants (e.g. in the leaves of green and black tea) and fungus. Results evidently demonstrated that L-theanine clearly has a pronounced effect on attention performance and reaction time response in normal healthy subjects susceptible to having high anxiety (Higashiyama et al., 2011).
A dose of L-theanine equivalent to eight cups of black tea improves cognitive and neurophysiological measures of selective attention, to a degree that is comparable with that of caffeine. The combination of Theanine and caffeine seem to have additive effects on attention in high doses (Kahathuduwa et al.,2016).
Studies suggest that 97 mg of L-theanine in combination with 40 mg of caffeine helps to focus attention during a demanding cognitive task (Giesbrecht 2010).

Bacopa Monnieri
Bacopa Monnieri is an herb which has been used in Ayurvedic medicine for centuries. Bacopa's primary mechanism of action is still unclear, it seems to be an anti-oxidant, a weak acetylcholinesterase inhibitor and a cerebral blood flow activator (Aguiar & Borowski , 2013).
There is some evidence to suggest that Bacopa Monnieri improves memory with little evidence of enhancement in any other cognitive domains (Pase et al., 2012).

Piracetam
Closing the circle to the beginning of this short introduction to the topic: Giurgea
first coined the term "nootropic" when he synthesized Piracetam in 1964. Since it is not approved by the US FDA, it is primarily used in Europe, Asia, and South America. It is commonly prescribed for cognitive impairment and dementia in several countries of Europe. Research suggests that Piracetam might also have a positive effect on healthy individuals. Subjects were given 3×4 capsules at 400 mg per day, in a double blind study. Each subject learned series of words presented as stimuli upon a memory drum. No effects were observed after 7 days but after 14 days verbal learning had significantly increased (Dimond & Brouwers, 1976).
It might also be beneficial for cognitive decline associated with age. Aging subjects did significantly better in a computerized perceptual-motor tasks when on piracetam than on a placebo. (Mindus et al. 1976).
While these old studies may not be that reliable, it is still held that
Piracetam's “efficacy is documented in cognitive disorders and dementia, vertigo, cortical myoclonus, dyslexia, and sickle cell anemia. While high doses are sometimes necessary, piracetam is well tolerated” (Winblad, 2005).
Since Piracetam was first synthesized many structurally similar compounds have emerged. These so called Racetams have poorly understood mechanisms of action; however, piracetam and aniracetam are known to act as positive allosteric modulators of AMPA receptors and appear to modulate cholinergic systems (Gualtieri et al., 2002).

This article is solely for information purposes, not a substitute for professional medical or dietary advice.
The provisos of the LongeCity user agreement apply.write
for LongeCity

by undefined @ Canadian CattlemenCanadian Cattlemen

Fri Feb 02 12:34:04 PST 2018

Many cows came home in 2017 from pastures parched by drought for much of the grazing season. Without proper supplementation of brood cows through the rest of their gestation, vitamin and mineral deficiencies will show up as health issues next spring with economic consequences that often persist for several more. It is well established that […] Read more

by Owen Alexander @ Alt Protein

Sat Dec 30 11:05:13 PST 2017

Whey protein supplements might just be the most popular supplement consumed. Together with multivitamins and fish oil, it is a ‘staple’ supplement that even the most casual of fitness enthusiasts would likely have consumed. Because of this popularity, there must be dozens of whey protein brands on the market, each attempting to differentiate itself in ... Read moreMammoth Whey Review: Is This the Supplement for You?

by GIS @ Gastrointestinal Society

Thu May 25 14:37:09 PDT 2017

Have you been diagnosed with Crohn's disease or ulcerative colitis? Do you want to get into running but don’t want to train alone? Would you like a reason to get outside and become healthier and more physically active? If so, the Gastrointestinal Society’s brand-new running clinic for people with active Crohn's disease or ulcerative colitis [...]

Help me choose a probiotic for histamine intolerance issue - posted in Supplements: Wow, I thought all probiotics were the same.Had no idea there were so many choices. I believe I have a histamine tolerance issue (rash around eyes when drinking alcoholic or fermented beverages(Kombucha) ao am looking for a probiotic that helps to suppress histamines. My understanding is that most yogurt and probiotics have just the opposite effect.After reading several articles I believe I need a pr...

by undefined @ Canadian CattlemenCanadian Cattlemen

Tue Feb 06 08:16:26 PST 2018

Canadian Cattlemen’s Association (CCA) leadership travelled to two major agriculture policy conventions in the United States in early January to promote common interests in the North American Free Trade Agreement (NAFTA) and urge progress on regulatory modernization to improve the flow of trade between the two countries. The advocacy efforts are part of an increasingly […] Read more

by undefined @ Canadian CattlemenCanadian Cattlemen

Mon Feb 12 08:52:12 PST 2018

That first feeding of colostrum invariably charts the course for a calf’s future success and profitability. Knowing that the dam’s udder and teat structure is important to a successful first feeding Kajal Devani, is aiming to improve the genetic selection for improved mammary conformation in Canadian Angus cattle. Devani, who is the Canadian Angus Association’s […] Read more

by @ ImmInst Active Topics

Fri Feb 09 05:41:57 PST 2018

I've been testing a few drops of lavender essential oil for my sky-high levels of anxiety. This stuff is potent. I took 8 drops today, and it's almost as efficient as 100mg of pregabalin ( I've been taking up to 400 mg of pregabalin daily these last months for anxiety and insomnia ). Make sure it's for oral consumption , some essential oils are for use diluted on skin only. Mix the drops with something fat , or just take it in water . It did create some heartburn though, but I took a very high dosage.

I've also taken Silexan ( an extract of lavender ) before. It's bloody expensive, and cheap lavender oil works just as well.

Interestingly, lavender essential oil seems to work the same way as pregabalin :

Recent clinical data support the clinical use of oral lavender oil in patients suffering from subsyndromal anxiety. We identified the molecular mechanism of action that will alter the perception of lavender oil as a nonspecific ingredient of aromatherapy to a potent anxiolytic inhibiting voltage dependent calcium channels (VOCCs) as highly selective drug target. In contrast to previous publications where exorbitant high concentrations were used, the effects of lavender oil in behavioral, biochemical, and electrophysiological experiments were investigated in physiological concentrations in the nanomolar range, which correlate to a single dosage of 80 mg/d in humans that was used in clinical trials. We show for the first time that lavender oil bears some similarities with the established anxiolytic pregabalin. Lavender oil inhibits VOCCs in synaptosomes, primary hippocampal neurons and stably overexpressing cell lines in the same range such as pregabalin. Interestingly, Silexan does not primarily bind to P/Q type calcium channels such as pregabalin and does not interact with the binding site of pregabalin, the α2δ subunit of VOCCs. Lavender oil reduces non-selectively the calcium influx through several different types of VOCCs such as the N-type, P/Q-type and T-type VOCCs. In the hippocampus, one brain region important for anxiety disorders, we show that inhibition by lavender oil is mainly mediated via N-type and P/Q-type VOCCs. Taken together, we provide a pharmacological and molecular rationale for the clinical use of the oral application of lavender oil in patients suffering from anxiety.

Bacteria in your digestive tract can be good or bad, according to the website Best Probiotic. It quotes the Royal Academy of Medicine England as blaming an imbalance between good and bad bacteria for causing 80 percent of all degenerative diseases. Probiotic supplements with "good" bacteria have become increasingly popular. They can aid...

by @ Articles

Sun Mar 08 16:35:01 PDT 2015

While the idea that drastic life extension may be an option for humankind in the future has been encountered by many through the media and fiction, the vast majority of the public do not grasp whether and how this could realistically apply to them or their loved ones.

Some argue that since life is an universally desirable good and age-related suffering and death universally feared and avoided, ‘public perception’ is something that will take care of itself. If anything, the inherent attractiveness of the concept will always guarantee media interest perhaps even to the point of generating unwarranted hype and the empty promises that have been the bane of the scientific life extension movement for centuries.

Others argue, with great conviction, that public perception and ‘marketing a life extension movement’ should be a prime objective. Here is a list of eight reasons why:

1. Broaden the pool of ideas. Generally, the more minds are altered to and focused towards a common objective, the greater the chance than innovative or groundbreaking ideas will be generated. If Life Extension is a more broadly known, accepted and prestigious topic of interest, more bright minds will be attracted to it.

2. Increase public sector funding and donations. As businesses tend to fund research only when profitability is close it often falls to the public sector and philanthropists to fund the "starter end" of research that will eventually lead to usable products which business will then want to take up.

3. Reduce opposition. There is an element of ‘shock’ associated with the concept that aging and death may not be inevitable which can lead to denial or impatient dismissal. Visceral or ideological opposition to life extension translates into less government funding, less scientific interest, less favorable laws and less industry support especially if there is no widely established counter-position.

4. Improve regulation. Whether we are thinking about laws allowing or prohibiting life extension treatments in general, or the speed and efficiency at which the FDA similar entities conduct their reviews, the support of government agencies is important at every stage of the process of getting treatments to the public. Responsive regulation can be generated through public pressure and media attention.

5. Focus corporate interests towards effective treatments. Only if there is a clear and well-informed demand for proven and validated treatments will effective products become more profitable to the industry than ineffective ‘snake oil’.

6. Build economies of scale. Given the urgent need for life extension treatments for many people there is an interest in helping to bring costs down as soon as possible. If pent-up public demand becomes more clearly visible, consideration of scale-up will become a part of more business plans and healthcare reforms.

7. Improve public health. A focus on life extension often comes with increased health consciousness. Prevention is better and cheaper than cures and if more people participate in a wider programme of health-conscious living, this is likely to bring overall healthcare costs down.

8. Reduce social unrest and disruption. Even once society accepts the concept of life extension and associated treatments there will still be people who are unwilling or unable to participate. Moreover, extended lifespans will affect society profoundly. Careful public engagement ensures that social unrest and discrimination can be minimised.

If at least one of these reasons makes sense to you, then you may want to think about how you could help ‘connect’ the LongeCity’s mission with others. Generally, the ‘self-multiplying’ effect of outreach should not be underestimated. People act as role models and influencers of their peers. Beyond all media spin, if a person acts and speaks with conviction, others will take note; and if people realize that their friends and family members could live longer they will be more willing to engage in the idea themselves.

by life extension @ Alivebynature – Evidence Based Reviews

Fri Jan 12 12:47:12 PST 2018

Scientists are discovering new ways that NAD+ facilitates healthy longevity.1-3 NAD+ levels markedly decline with age, creating an energy deficit that decreases the body’s ability to retain youthful function.4 To give you an idea how impactful NAD+ can be, by age 50 a typical person may have only half the NAD+ they did in youth. […]

by undefined @ Canadian CattlemenCanadian Cattlemen

Thu Feb 08 10:44:33 PST 2018

Honouring a Farmer-Poet By Kerry Wood, Red Deer, Alta. Four hundred farmers and their families met on Labor Day to stage one of the most unique ceremonies ever held in Western Canada, when the pioneer Icelandic community of Markerville in Central Alberta unveiled a monument honoring the famous farmer-poet, Stephan G. Stephansson. Dominion, provincial, and […] Read more

by @ LongeCityNews

Does walking 20 miles a day with a 1 to 2 thousand foot elevation gain for about 120 days in a row increase health and promote a longer lifespan?

All sorts of longevity studies suggest that this may be the case and my subjective personal experience tells me this is true, but I have no way to measure it.

If it were possible to physically measure the effects of a long distance hike it might become possible to identify ways to improve it and make it easier for others to enjoy these benefits – on and off the trail.

I would like to offer my upcoming 3rd thru-hike of the 2,650 mile long Pacific Crest Trail for a legitimate researcher to study. Am open to some level of experimentation, mostly in improved diet, and possibly with life extension products.

Am 63 years old. In basically good health and physical fitness. Maintain a reasonably healthy diet. I am fully geared up, have the trip planned out and am able to finance it out of pocket. I am not looking for someone to subsidize the hike unless time or costs are increased beyond what my estimate of a normal hike would require.

In the event that no researcher is interested, the following is a list of benefits which I associate with long distance hiking. Readers of this forum are encouraged to comment on it and add to it.

1) This sort of walking doubles and sometimes triples the demand for calories. Due to backpack weight restrictions, it is impossible to carry as much food as a hiker would like to have. As a result, hikers sort of starve their way to the next resupply point. Within a month this becomes a semi-permanent condition called hiker hunger. Is this a kind of calorie restricted diet?

2) Walking seems like the perfect form of exercise. At 20 miles a day plus elevation gain, does this produce an equivalent to the Jack LaLanne level of exercises he thought was needed for health and longevity?

3) Seems like all of the automatic functions such as digestion, blood circulation, perspiration, breathing and etc appear to operate better than normal all day long. While walking, it is also easy to monitor body functions and balance things out when needed, such as resting or drinking water or taking in nutrition or eliminating.

4) Being outdoors all day long in wide temperature and weather variations, surrounded by panoramic views, listening to nature sing, breathing freshly produced oxygen, drinking unadulterated water from the source and etc have long been known for its health benefits. What happens when this becomes the default norm over a 5 month period?

5) Seems like most stress comes from toxic people, life burning cultural situations and financial - political chaos. On the trail, its pretty much all gone. This alone would add years to anyone’s lifespan. How is this sort of thing measured?

6) The daily hike frequently becomes a kind of walking meditation. I particularly enjoy how the avalanche of accumulated experience almost automatically sorts itself out so that the truly important matters are then easier to think about. Is there a link between disorganized, undigested memories and physical brain degeneration?

7) After a full day on the trail, hikers lay their exhausted, sore bodies down to get 8 to 10 hours of sleep each night and arise in the morning at very high levels of recovery. Sleeping directly on the ground appears to have the same effect that household earthing gear produces (duh). How to measure this?

8) Obviously there is more. Obviously each of these will have some positive benefit. But what is the effect of all of it together? Can these benefits be carried over from the trail into ‘real life’? (don't get me started) Can these benefits help non hikers?

by Lisa Richards @ The Candida Diet

Wed Feb 07 15:24:07 PST 2018

As most of us know, probiotics are a great way to improve gut health. Many scientific studies have shown that taking probiotic supplements or eating fermented foods can lead to better digestion, healthy elimination, and a stronger immune system. These benefits are crucial to the daily maintenance of the body and its many functions. Your […]

by @ Action

Does walking 20 miles a day with a 1 to 2 thousand foot elevation gain for about 120 days in a row increase health and promote a longer lifespan?

All sorts of longevity studies suggest that this may be the case and my subjective personal experience tells me this is true, but I have no way to measure it.

If it were possible to physically measure the effects of a long distance hike it might become possible to identify ways to improve it and make it easier for others to enjoy these benefits – on and off the trail.

I would like to offer my upcoming 3rd thru-hike of the 2,650 mile long Pacific Crest Trail for a legitimate researcher to study. Am open to some level of experimentation, mostly in improved diet, and possibly with life extension products.

Am 63 years old. In basically good health and physical fitness. Maintain a reasonably healthy diet. I am fully geared up, have the trip planned out and am able to finance it out of pocket. I am not looking for someone to subsidize the hike unless time or costs are increased beyond what my estimate of a normal hike would require.

In the event that no researcher is interested, the following is a list of benefits which I associate with long distance hiking. Readers of this forum are encouraged to comment on it and add to it.

1) This sort of walking doubles and sometimes triples the demand for calories. Due to backpack weight restrictions, it is impossible to carry as much food as a hiker would like to have. As a result, hikers sort of starve their way to the next resupply point. Within a month this becomes a semi-permanent condition called hiker hunger. Is this a kind of calorie restricted diet?

2) Walking seems like the perfect form of exercise. At 20 miles a day plus elevation gain, does this produce an equivalent to the Jack LaLanne level of exercises he thought was needed for health and longevity?

3) Seems like all of the automatic functions such as digestion, blood circulation, perspiration, breathing and etc appear to operate better than normal all day long. While walking, it is also easy to monitor body functions and balance things out when needed, such as resting or drinking water or taking in nutrition or eliminating.

4) Being outdoors all day long in wide temperature and weather variations, surrounded by panoramic views, listening to nature sing, breathing freshly produced oxygen, drinking unadulterated water from the source and etc have long been known for its health benefits. What happens when this becomes the default norm over a 5 month period?

5) Seems like most stress comes from toxic people, life burning cultural situations and financial - political chaos. On the trail, its pretty much all gone. This alone would add years to anyone’s lifespan. How is this sort of thing measured?

6) The daily hike frequently becomes a kind of walking meditation. I particularly enjoy how the avalanche of accumulated experience almost automatically sorts itself out so that the truly important matters are then easier to think about. Is there a link between disorganized, undigested memories and physical brain degeneration?

7) After a full day on the trail, hikers lay their exhausted, sore bodies down to get 8 to 10 hours of sleep each night and arise in the morning at very high levels of recovery. Sleeping directly on the ground appears to have the same effect that household earthing gear produces (duh). How to measure this?

8) Obviously there is more. Obviously each of these will have some positive benefit. But what is the effect of all of it together? Can these benefits be carried over from the trail into ‘real life’? (don't get me started) Can these benefits help non hikers?

by undefined @ Canadian CattlemenCanadian Cattlemen

Mon Nov 07 12:56:11 PST 2016

Corn is a powerful and versatile feed that can carry your herd through winter if you do a few things properly to get the crop off to a good start, says Breeanna Kelln, DuPont Pioneer’s livestock information manager for Western Canada. While corn is still a relatively new crop in the West, interest in silage […] Read more

by Joe (MSc Nutrition), Dietitian @ DIET vs DISEASE

Tue Feb 06 08:21:47 PST 2018

[Last updated 10th February, 2018] Histamine intolerance is poorly understood in the medical world. Most health professionals are not knowledgeable on the topic; diagnosis is flaky at best; and the condition itself is difficult to treat. That’s why I’ve created this guide. It’s a comprehensive, research-driven review of histamine intolerance, with a particular emphasis on [Discover More...]

by @ Health

Sun Feb 11 17:35:26 PST 2018

Hey everyone,

Thank you in advance for taking the time to read and respond to my post. I’m a 23 year old (otherwise healthy) male who was diagnosed with lyme disease about two months ago. After undergoing an intense supplement/herbal/energetical therapy cleanse and detox, my docotor confirmed that the lyme had left my body. However, I am still experiencing all of my original symptoms, including random shaking, a neck tremor, intense brain fog, a really infammed gut/liver/kidneys, etc. I’m struggling to determine my next course of action — has anyone reading his post dealt with lyme? — have you tried dietary changes to help heal your system? I’m also curious if bpc 157 would be a good option for me? I already eat a fairly well balanced diet that is exclusively organic/non gmo, as well as taking about 15 relevant supplents a day (including probiotics). I guess, in general, I’m seeking any lyme, dietary, or other advice that you might have for me.

by undefined @ Canadian CattlemenCanadian Cattlemen

Tue Oct 03 11:50:15 PDT 2017

By scientific estimate, ticks have been around for 100 million years. They represent the most famous blood-sucking arachnids, (eight-legged organisms). The world is now in unchartered territory when it comes to infectious diseases. Over the past century, the number of new infectious diseases cropping up each year has nearly quadrupled. The number of outbreaks per […] Read more

Pharmaceutical interventions can slow aging in animals, and have advantages because their dose can be tightly regulated and the timing of the intervention can be closely controlled. They also may complement environmental interventions like caloric restriction by acting additively. A fertile source for therapies slowing aging is FDA approved drugs whose safety has been investigated. Because drugs bind to several protein targets, they cause multiple effects, many of which have not been characterized. It is possible that some of the side effects of drugs prescribed for one therapy may have benefits in retarding aging. We used computationally guided drug screening for prioritizing drug targets to produce a short list of candidate compounds for in vivo testing. We applied the virtual ligand screening approach FINDSITEcomb for screening potential anti-aging protein targets against FDA approved drugs listed in DrugBank. A short list of 31 promising compounds was screened using a multi-tiered approach with rotifers as an animal model of aging. Primary and secondary survival screens and cohort life table experiments identified four drugs capable of extending rotifer lifespan by 8-42%. Exposures to 1 µM erythromycin, 5 µM carglumic acid, 3 µM capecitabine, and 1 µM ivermectin, extended rotifer lifespan without significant effect on reproduction. Some drugs also extended healthspan, as estimated by mitochondria activity and mobility (swimming speed). Our most promising result is that rotifer lifespan was extended by 7-8.9% even when treatment was started in middle age.

by @ LongeCityNews

Fri Feb 09 16:00:03 PST 2018

The tissue engineering and regenerative medicine communities are too large and energetic to do more than sample their output, or note the most interesting advances that stand out from the pack. The publicity materials I'll point out here are a recent selection of items that caught my eye as they went past. Dozens more, each of which would have merited worldwide attention ten or fifteen years ago, drift by with little comment every year. The state of the art is progressing rapidly towards both the ability to build complex tissues from a cell sample, such as patient-matched organs for transplantation, and the ability to control regeneration and growth inside the body. Ultimately we may not need transplantation if native organs can be persuaded to repair themselves ... but this will likely also require significant progress towards repairing the cell and tissue damage of aging, the forms of molecular breakage that degrade regenerative capacity.

Even though the research community has progressed a long way past the capabilities of even a decade ago, there remains a longer road ahead. Transplants of cell populations are still very challenging; only a small fraction of those cells survive to take up residence and contribute over the long term. The best technology demonstrations manage 10% survival or thereabouts. Standard approaches to finding the best methodology for each cell type and situation have yet to arise. There is a lot of trial and error. Yet replacement of cell populations, reliably, and with high quality, youthful, undamaged cells, is needed to treat many of the consequences of aging. Consider the loss of dopamine-generating neurons in Parkinson's disease, for example, or the wearing down of the stem cell population responsible for generating the immune system, or the structural remodeling and weakening of the heart in response to hypertension. Removing the damage that caused those issues will not automatically restore all of the losses.

For the first time, researchers have regenerated patients' damaged lungs using autologous lung stem cell transplantation in a pilot clinical trial. In 2015, the researchers identified p63+/Krt5+ adult stem cells in a mouse lung, which had potential to regenerate pulmonary structures including bronchioles and alveoli. Now they are focusing on lung stem cells in humans rather than mice. The researchers found that a population of basal cells labeled with an SOX9+ marker had the potential to serve as lung stem cells in humans. They used lung bronchoscopy to brush off and amplify these lung stem cells from tiny samples.

In order to test the capacity of lung stem cells to regenerate lung tissue in vivo, the team transplanted the human lung stem cells into damaged lungs of immunodeficient mice. Histological analysis showed that stem cell transplantation successfully regenerated human bronchial and alveolar structures in the lungs of mice. Also, the fibrotic area in the injured lungs of the mice was replaced by new human alveoli after receiving stem cell transplantation. Arterial blood gas analysis showed that the lung function of the mice was significantly recovered.

The team launched the first clinical trial based on autologous lung stem cell transplantation for the treatment of bronchiectasis. The first two patients were recruited in March 2016. Their own lung stem cells were delivered into the patients' lung through bronchoscopy. One year after transplantation, two patients described relief of multiple respiratory symptoms such as coughing and dyspnea. CT imaging showed regional recovery of the dilated structure. Patient lung function began to recover three months after transplantation, which maintained for one year.

Kidney glomeruli - constituent microscopic parts of the organ - were generated from human embryonic stem cells grown in plastic laboratory culture dishes containing a nutrient broth known as culture medium, containing molecules to promote kidney development. They were combined with a gel like substance, which acted as natural connective tissue - and then injected as a tiny clump under the skin of mice. After three months, an examination of the tissue revealed that nephrons: the microscopic structural and functional units of the kidney - had formed.

Tiny human blood vessels - known as capillaries - had developed inside the mice which nourished the new kidney structures. However, the mini-kidneys lack a large artery, and without that the organ's function will only be a fraction of normal. So, the researchers are working with surgeons to put in an artery that will bring more blood the new kidney. "We have proved beyond any doubt these structures function as kidney cells by filtering blood and producing urine - though we can't yet say what percentage of function exists. What is particularly exciting is that the structures are made of human cells which developed an excellent capillary blood supply, becoming linked to the vasculature of the mouse. Though this structure was formed from several hundred glomeruli, and humans have about a million in their kidneys - this is clearly a major advance. It constitutes a proof of principle - but much work is yet to be done."

Researchers have created a new lab-grown blood vessel replacement that is composed completely of biological materials, but surprisingly doesn't contain any living cells at implantation. The vessel, that could be used as an "off the shelf" graft for kidney dialysis patients, performed well in a recent study with nonhuman primates. It is the first-of-its-kind nonsynthetic, decellularized graft that becomes repopulated with cells by the recipient's own cells when implanted.

The researchers generated vessel-like tubes in the lab from post-natal human skin cells that were embedded in a gel-like material made of cow fibrin, a protein involved in blood clotting. Researchers put the cell-populated gel in a bioreactor and grew the tube for seven weeks and then washed away the cells over the final week. What remained was the collagen and other proteins secreted by the cells, making an all-natural, but non-living tube for implantation.

To test the vessels, the researchers implanted the 15-centimeter-long (about 5 inches) lab-grown grafts into adult baboons. Six months after implantation, the grafts grossly appeared like a blood vessel and the researchers observed healthy cells from the recipients taking up residence within the walls of the tubes. None of the grafts calcified and only one ruptured, which was attributed to inadvertent mechanical damage with handling. The grafts after six months were shown to withstand almost 30 times the average human blood pressure without bursting. The implants showed no immune response and resisted infection.

by Ken Silvers @ Probiotics Center

Sun Oct 08 01:53:11 PDT 2017

Doctor’s Best Betaine HCL Pepsin & Gentian Bitters is another well-composed supplement from this company. I have reviewed several of Doctor’s Best supplements and always found them of high quality. Therefore, most people do respond well to the high-quality enzymes included in Doctor’s Best. However, some people have specific needs and might need to try different digestive enzyme supplements to find one with a composition that fits […]

everyone talks about bio gaia drops, has anyone tried Jamieson Baby Probiotic drops? I assume they would serve the same purpose? They are a lot more cost efficient and available now, whereas the bio gaia I would have to order it in and it costs twice as much. Also, are the Jamieson ones refrigerated also?

Finding a good probiotic will help you maintain a healthy balance of bacteria in your digestive tract and even boost your immune system. Whether or not you have Candida overgrowth, a probiotic supplement can be a great addition to your diet. I’ve been using probiotics for a while now, so I’ve made a list of …

by @ Articles

Sun Aug 20 11:04:47 PDT 2017

When Darwin’s theory of evolution by natural selection was established, biologists were puzzled by the existence of senescence and aging among all organisms. Why did the evolutionary pressure not produce immortal species? They concluded that even the power of evolution has its limitations. It took almost hundred years to reach the idea that mortal individuals may be preferred by nature for following reasons — the genes resulting in advantage in early life might cause damage in late life, and the reproduction starts as soon as possible. Around the middle of twentieth century, there finally was a framework for the gerontological research conduced in the following decades — the first evolutionary theories of aging (Gavrilov & Gavrilova, 2002).
There are two major groups of theories aiming to explain the mechanism of aging, so-called programmed and error theories. The programmed ones are based on the senescence-causing nature of certain genes (these are also called evolutionary theories), hormones or the immune system. Error theories claim that we age because of general damage caused by cell weariness, metabolic rate, cross-linked proteins, free radicals or somatic DNA changes (Jin, 2010).
The beauty of various aging theories is that most of them are not mutually exclusive. We can see that newer theories do not necessarily oppose the old ones, but rather shed more light and offer more in-depth views on the process of senescence.
The pioneering idea from 1882 was Weismanns’s theory of programmed death (also called wear-and-tear theory) claiming something like apoptosis of the multicellular organism. Although disproved by experiments, his theoretical explanation of the mechanism predicted the discovery of Hayflick limit (Gavrilov & Gavrilova, 2002). According to Weismann’s first conception, nature priorities young individuals over elderly because of limited resources.
Pearl stated his ‘rate of living’ theory of aging in 1928, although the idea comes from Rubner who, in 1908, suggested that every organism has limited amount of metabolic energy and therefore its age depends on the rate of metabolism which correlates with organism’s size (Pearl, 1928). Most consider the rate of living theory to be flawed (Lints, 1989; de Magalhaes, Costa, & Church, 2007; Vaanholt, Daan, Schubert, & Visser, 2009).
A few decades later, the following evolutionary models have emerged:
Medawar’s hypothesis of mutation accumulation proposes that aging is a by-product of natural selection — genes causing senescence in later stadium of life cannot be eliminated because the genetic information was most likely already transferred to successors by individuals in their early adulthood (Gavrilov & Gavrilova, 2002). This theory from 1952 is considered the first modern theory of aging. Charlesworth confronted Medawar’s model with a discovery of late-life mortality plateaus and in 1994 presented so-called modified mutation accumulation theory (Charlesworth, 2001; Ljubuncic & Reznick, 2009).
In his antagonistic pleiotropy theory (also called ‘pay later’ theory), Williams in 1957 expressed the idea that even the same genes which cause trouble at advanced age may be advantageous in earlier stages of life, and therefore be not only tolerated, but even preferred by natural selection (Gavrilov & Gavrilova, 2002).
In 1979, Kirkwood extended this theory to the disposable soma theory — organisms may save energy by reducing accuracy in cells metabolism and invest it in faster development and reproduction (Kirkwood & Holliday, 1979). This is the last one of famous, genes-orientated evolutionary models.
The following can be classified as programmed theories:
The neuroendocrine theory proposed in 1954 by Dilman says that the main cause of aging is a loss of receptor sensitivity of the hypothalamus over time, and therefore its control of adequate production of hormones declines which leads to ineffectiveness and lower hormone levels in organism. It is an attempt to explain a high occurrence of degenerative diseases in late age (“Neuroendocrine Theory of Aging: Chapter 1,” 1999). Research on hormonal signaling pathways confirms that hormone levels have at least a partial role in determining longevity (van Heemst et al., 2005).
In 1964, Walford suggested his immunologic theory of aging — due to increasing diversity of cells, the immune system looses its efficiency with age which leads to insufficient responses against pathogens as well as to autoimmune reactions against self proteins (Walford, 1964).
All following attempts to explain the mechanism behind a process of aging are usually called error or damage theories.
Bjorksten’s "crosslinkage theory" says that proteins become linked together in presence of certain crosslinking agents, and after some time, accumulation of these molecular aggregates causes decline in tissue functions. This theory from 1942 is no longer popular (Bjorksten, 1968). Later research has showed that advanced glycation end products (AGEs) accumulate in collagen and lead to outcomes predicted by Bjorksten (Verzijl et al., 2002; Aronson, 2003).
These days very popular among researchers and public, the free radical theory was suggested by Harman in 1956. His idea was that the occurrence of free radicals, or reactive oxygen species naturally produced in living organisms, leads to macromolecular damage which accumulates and causes physiological changes known as senescence (Harman, 2009). Later he suggested the reactive oxygen species formation takes place mainly in mitochondria which causes a decline in important mitochondrial functions (Harman, 1972). Because of the theory’s popularity, various extensions of Harman’s model were created, usually considering different sites as a main target of free radicals.
Failla’s somatic mutation theory from 1958 posits that increasing number of mutations of genetic material causes a decrease in cellular, organ and body functions (Failla, 1958; Gensler & Bernstein, 1981; Kennedy, Loeb, & Herr, 2012). The theory received a lot of criticism in previous decades (Vijg, 2000). Kaya, Lobanov and Gladyshev (2015) investigated aging in yeast and failed to find evidence in support of Failla’s thesis.
Orgel proposed his error catastrophe theory in 1963. He saw the cause of aging in accumulation of malfunctioning proteins coming from errors during protein translation (Orgel, 1963). This theory never gained popularity and was soon disproved (Gershon & Gershon, 1976).
Alexander in 1967 extended Failla’s theory by hypothesizing that DNA damage instead of mutation is the cause of aging (Alexander, 1967). These days, this version called
"somatic DNA damage theory of aging" is more often used by scientists (Freitas & de Magalhaes, 2011; Soares et al., 2014). Evidence suggests that more damage happens in mitochondrial DNA than in nuclear DNA (Ames, 2009).
In 2002, Brunk and Terman published the mitochondrial-lysosomal axis theory. It states that defective macromolecules derived from mitochondria undergo further changes in lysosomes to become lipofuscin inclusions. These end products decrease cell’s autophagocytotic capacity which leads to more mitochondrial defects (Brunk & Terman, 2002).
Zs.-Nagy’s "membrane hypothesis" focuses on a decline of mitochondrial functions due to lessened membrane permeability caused by residual heat coming from nerve signals as well as by reactive oxygen species (Zs.-Nagy, 2014).
Recent versions of damage theories claim that free radicals are only one kind of senescence-causing by products of metabolism but the real initiator of all the inevitable damage is biological imperfectness. In other words, there are always types of damage which lack adequate repair mechanisms in organism and the most severe source of errors depends on actual conditions (Gladyshev, 2013; Gladyshev, 2014). This idea comes from the
"reliability theory", which focuses on systems failure in machines (Gavrilov & Gavrilova, 2001).
In spite of many research programs and lots of scientists involved, the unifying factor in aging is at the moment still unknown.

References

Alexander, P. (1967). The role of DNA lesions in the processes leading to ageing in mice. Symp Soc Exp Biol, 21, 29-50.

Orgel, L. (1963). The Maintenance of the Accuracy of Protein Synthesis and its Relevance to Ageing. Proceedings Of The National Academy Of Sciences, 49(4), 517-521.
http://dx.doi.org/10.1073/pnas.49.4.517

by undefined @ Canadian CattlemenCanadian Cattlemen

Mon Feb 12 08:27:12 PST 2018

Piper Whelan of Airdrie, Alta., is the new field editor for Canadian Cattlemen. Raised on a purebred Maine-Anjou ranch at Irricana, Whelan studied English and history at the University of Alberta and journalism at the University of King’s Col­­lege. She previously worked in publishing and as a registry assistant for the Canadian Charolais Association, and […] Read more

by undefined @ Canadian CattlemenProving the potential of probiotics in beef cattle – Canadian Cattlemen

Mon Oct 05 11:28:30 PDT 2015

Caution is the word for now from an Alberta intestinal health research group on products claimed to have prebiotic or probiotic activity to promote health benefits for people and livestock. Use of these products won’t harm cattle or people. The worst that could happen from a production standpoint is that they will increase costs with […] Read more

by Ken Silvers @ Probiotics Center

Wed Apr 26 21:02:18 PDT 2017

CocoBiotic by Body Ecology is a naturally fermented drink. It includes a gut friendly mix of coconut water, grains, beneficial bacteria and prebiotic fiber. This is indeed a refreshing and addictive sparkling drink! CocBiotic is another superb, high-quality product from this company. I can understand why CocoBiotic has become so popular—it’s a refreshing, mild and fizzy drink […]

by alina pilani @ Alivebynature – Evidence Based Reviews

Thu Jan 04 06:51:51 PST 2018

It has long been known that foods affect blood sugar levels differently. However, individual factors may also play a role. People respond differently to foods, even when eating the exact same thing. For this reason, a team of scientists studied these individual factors. Then, they developed an algorithm to predict blood sugar responses to meals. Here is […]

by lassesen @ CFS Remission

Thu Feb 08 21:36:10 PST 2018

A reader asked: “Do you still think thick blood is a common issue and do you still recommend getting the multiple labs for thick blood? Is there a viscosity test you recommend for seeing that the thickness is at any given time?” Given that I have been focusing on the microbiome (mainly because it is actionable […]

by undefined @ Canadian CattlemenCanadian Cattlemen

Fri Feb 02 12:34:04 PST 2018

Many cows came home in 2017 from pastures parched by drought for much of the grazing season. Without proper supplementation of brood cows through the rest of their gestation, vitamin and mineral deficiencies will show up as health issues next spring with economic consequences that often persist for several more. It is well established that […] Read more

by @ Articles

is led by life-extension trailblazer Kelsey Moody. It is interesting that he turns the attention of his new venture Ichor Therapeutics to the potential health effects of 'buckyballs' - a topic that has received significant attention on LongeCity ever since it was claimed in a scientific report that rats fed on olive oil infused with these structures experience dramatically increased maximal lifespans. (Review here). True to it mission, LongeCity hosts the leading international discussion forum on this topic. Previously, the LongeCity community has come together to fund further grassroots research on C60 in mice and these studies are on-going.

Meanwhile though, in keeping with the pioneer spirit often found on the LongeCity forums, reports have come in from people trialing C60 in olive oil on themselves. As Kelsey points out, the long-term safety of this has yet to be established, and this project is particularly interested in whether C60 in olive oil has any cancer-inducing properties. Conversely, it may be the case that the compound has a tumor–suppressing function. To investigate this, the team plans to infuse a total of 25 mice with C60-olive oil of various strengths or with an inert ‘control’ solution, graft a human cancer cell line to the mice and study the results. (Full research proposal here)

If the fundraiser succeeds it will further support the revolutionary notion of stakeholder-oriented, grass-roots science which complements, challenges and enriches academic research at those junctures that the community actually cares about. Moreover and perhaps even more importantly the fundraiser will help to built capacity and community interface at a dedicated life-extension research facility. Already, Ichor has housed an intern on a LongeCity stipend (Report here- Members only). Ultimately, we hope to create a network of such community-friendly labs around the globe, to provide aspiring young scientistswith training and networking and all members with easily accessible sources of expert advice.

LongeCity has facilitated 'crowdfunding' well before many other platforms in use today. This year, we have decided to try to tap into the potential of these external sites, but to add something to the process: This project is the first one to run on an external fundraising page that has received an official ‘stamp of endorsement’ from LongeCity.The team has mooted the project at LongeCity, submitted for formal peer review and informal members comments and the board looked into the ability of the team to use the donated money responsibly and to deliver success (Internal link here). In the end, the project received a high rating of 3 stars and LongeCity decided to match each dollar donation from our general funds. And, awesomely, a generous Member immediately stepped forward to match them as well!

by undefined @ Canadian CattlemenCanadian Cattlemen

Thu Jan 18 11:42:35 PST 2018

[UPDATED: Jan. 23, 2018 with ‘COMMENT’ at bottom] January 2018. The global economy is improving. The U.S. economy, drawing on Trump optimism, anticipated tax reform and more competitive American businesses seeing some profits, which should benefit Canadian businesses. U.S. beef demand is holding up decently in the face of increased supply. The 800-pound gorilla in […] Read more

• Science support: contribution to a scientific experiment that can be carried out in a short period of time with limited resources. The experiment should be distinguishable from the research that is already funded by other sources. This could be a side-experiment in an existing programme, a pilot experiment to establish feasibility, or resources for an undergrad or high-school student.

• Chapters support: organising a local
meetings. LongeCity could contribute to the room hire, the expenses of inviting a guest speaker or even the bar tab.

• Travel support: attendance at conferences, science fairs etc where you are presenting on a topic relevant to LongeCity. Generally this will involve some promotion of the mission and/or a report on the then conference to be shared with our Members

• Grant writing: Bring together a team of scientists and help them write a successful grant application to a public or private funding body. Depending on the project, the award will be a success premium or sometimes can cover the costs of grant preparation itself.

• Outreach: Support for a specific initiative raising public awareness of the mission or of a topic relevant to our mission. This could be a local event, a specific, organised direct marketing initiative or a media feature.

• Articles: Write a featured article for the LongeCity website on a topic of interest to our members or visitors. We are mainly looking for articles on scientific topics, but well-researched contributions on a relevant topic in policy, law, or philosophy are also welcome.
For
more info see here.

The small grants scheme includes 'micro grants' - up to $180 and 'small grants' - up to $500.
(Grant applications exceeding $500 would usually be expected to be 'matching fundraisers' discussed above.)

Decisions as part of the small grants programme are usually pretty quick and straightforward. However please contact us with a proposal ahead of time - we will not consider applications where the expenditure has already been incurred!
Proposals can be as short or elaborate as necessary, but normally should be about half a page long.

Only LongeCity Members can apply, but any Member is free to apply on behalf of someone else - thus, non-Members are welcome to find a Member to 'sponsor' their application.

by Owen Alexander @ Alt Protein

Mon Jan 22 10:51:12 PST 2018

Nowadays, raw juice detox programs are very popular and a good way to detoxify your body and lose weight. One option is to buy an excellent but expensive blender and prepare the juices yourself. This will, however, take time because you need to wash the ingredients, then peel and cut them into smaller pieces, and ... Read moreThe Raw Generation Skinny Cleanse Review: Does it Work as Promised?

by @ LongeCity - Articles

Sun Jun 19 18:16:58 PDT 2016

The Longecity “Affiliate Labs” are small, research-focused enterprises or
independent academic research groups led by a scientists with strong ties to the Longecity community and a proven track record of commitment to scientific
inquiry directly relevant to the Longecity mission.These leaders and their colleagues are not just trailblazers in advancing
important areas of regenerative and rejuvenation research, but also incredibly
helpful when there is a community need for peer review, when providing advice
and training to a young scientist, and in providing the expertise and tools to
test the novel, controversial, or promising scientific leads sourced from the
Longecity community and beyond.

Community Funding There is a small support fund that the labs can draw on to flexibly support
their research activities. While not a substitute for private investment and
public sector grants, the ability to flexibly ‘just try’ out a new idea without
needing to ‘pitch’ in lengthy proposals can be an invaluable accelerator to
research progress. All Affiliates have an active link to the Longecity
community, so there is a level of accountability and responsiveness beyond
anything encountered in ‘traditional’ research donations. By donating to the Affiliate Labs fund, Members can be assured that every penny
goes directly to an expert personally and professionally committed to making a
difference in the scientific conquest of death.
Donate HERE

by admin @ Alivebynature – Evidence Based Reviews

Thu Jan 18 07:09:27 PST 2018

Cellular health is a popular term in the health industry right now. The theory is that both your good health and your poor health is determined by the trillions of cells inside your body. This means that nutrients such as vitamins and minerals can help maintain good health if they are kept at the proper […]

by @ Articles

Sun Jun 19 18:16:58 PDT 2016

The Longecity “Affiliate Labs” are small, research-focused enterprises or
independent academic research groups led by a scientists with strong ties to the Longecity community and a proven track record of commitment to scientific
inquiry directly relevant to the Longecity mission.These leaders and their colleagues are not just trailblazers in advancing
important areas of regenerative and rejuvenation research, but also incredibly
helpful when there is a community need for peer review, when providing advice
and training to a young scientist, and in providing the expertise and tools to
test the novel, controversial, or promising scientific leads sourced from the
Longecity community and beyond.

Community Funding There is a small support fund that the labs can draw on to flexibly support
their research activities. While not a substitute for private investment and
public sector grants, the ability to flexibly ‘just try’ out a new idea without
needing to ‘pitch’ in lengthy proposals can be an invaluable accelerator to
research progress. All Affiliates have an active link to the Longecity
community, so there is a level of accountability and responsiveness beyond
anything encountered in ‘traditional’ research donations. By donating to the Affiliate Labs fund, Members can be assured that every penny
goes directly to an expert personally and professionally committed to making a
difference in the scientific conquest of death.
Donate HERE

by alina pilani @ Alivebynature – Evidence Based Reviews

Wed Jan 03 06:30:10 PST 2018

People who drink sugar-sweetened beverages tend to gain more weight over time. However, it is not known whether all types of sugar are equally fattening. For this reason, a team of scientists recently examined how different forms of sugar affect calorie intake. Here is a detailed summary of their results, published in the American Journal of […]

by GIS @ Gastrointestinal Society

Tue Sep 12 13:22:05 PDT 2017

Patients, Advocates and The Cameron Institute, issue call for equal access to IBD treatments CAMBRIDGE, ONTARIO (September 12, 2017) – Approximately 233,000 Canadians know how it feels to wake up every day with IBD (Inflammatory Bowel Disease), which includes Crohn’s Disease and Ulcerative Colitis – painful autoimmune disorders which attack the gastrointestinal tract.1,2 A new [...]

by @ LongeCity - Articles

Sun Mar 08 16:35:01 PDT 2015

While the idea that drastic life extension may be an option for humankind in the future has been encountered by many through the media and fiction, the vast majority of the public do not grasp whether and how this could realistically apply to them or their loved ones.

Some argue that since life is an universally desirable good and age-related suffering and death universally feared and avoided, ‘public perception’ is something that will take care of itself. If anything, the inherent attractiveness of the concept will always guarantee media interest perhaps even to the point of generating unwarranted hype and the empty promises that have been the bane of the scientific life extension movement for centuries.

Others argue, with great conviction, that public perception and ‘marketing a life extension movement’ should be a prime objective. Here is a list of eight reasons why:

1. Broaden the pool of ideas. Generally, the more minds are altered to and focused towards a common objective, the greater the chance than innovative or groundbreaking ideas will be generated. If Life Extension is a more broadly known, accepted and prestigious topic of interest, more bright minds will be attracted to it.

2. Increase public sector funding and donations. As businesses tend to fund research only when profitability is close it often falls to the public sector and philanthropists to fund the "starter end" of research that will eventually lead to usable products which business will then want to take up.

3. Reduce opposition. There is an element of ‘shock’ associated with the concept that aging and death may not be inevitable which can lead to denial or impatient dismissal. Visceral or ideological opposition to life extension translates into less government funding, less scientific interest, less favorable laws and less industry support especially if there is no widely established counter-position.

4. Improve regulation. Whether we are thinking about laws allowing or prohibiting life extension treatments in general, or the speed and efficiency at which the FDA similar entities conduct their reviews, the support of government agencies is important at every stage of the process of getting treatments to the public. Responsive regulation can be generated through public pressure and media attention.

5. Focus corporate interests towards effective treatments. Only if there is a clear and well-informed demand for proven and validated treatments will effective products become more profitable to the industry than ineffective ‘snake oil’.

6. Build economies of scale. Given the urgent need for life extension treatments for many people there is an interest in helping to bring costs down as soon as possible. If pent-up public demand becomes more clearly visible, consideration of scale-up will become a part of more business plans and healthcare reforms.

7. Improve public health. A focus on life extension often comes with increased health consciousness. Prevention is better and cheaper than cures and if more people participate in a wider programme of health-conscious living, this is likely to bring overall healthcare costs down.

8. Reduce social unrest and disruption. Even once society accepts the concept of life extension and associated treatments there will still be people who are unwilling or unable to participate. Moreover, extended lifespans will affect society profoundly. Careful public engagement ensures that social unrest and discrimination can be minimised.

If at least one of these reasons makes sense to you, then you may want to think about how you could help ‘connect’ the LongeCity’s mission with others. Generally, the ‘self-multiplying’ effect of outreach should not be underestimated. People act as role models and influencers of their peers. Beyond all media spin, if a person acts and speaks with conviction, others will take note; and if people realize that their friends and family members could live longer they will be more willing to engage in the idea themselves.

by undefined @ Canadian CattlemenCanadian Cattlemen

Mon Feb 05 12:41:02 PST 2018

Ontario cattlemen and the province have begun several programs to encourage more farmers to start raising beef in northern Ontario — where it is colder and the land is more suited to bush and cattle than corn and soybeans. Interest from producers considering a move north has been gaining momentum, and in mid-August 2017, the […] Read more

by undefined @ Canadian CattlemenCanadian Cattlemen

Tue Feb 06 08:05:50 PST 2018

The question of who land belongs to continues to haunt discussions around the world. In my international travels it most certainly was common to discuss not only land ownership but land access. For Canadians, ownership appears to be a given but the reality of land accessibility and ownership is a conversation we need to have. […] Read more

by @ Articles - Articles

The oldest human recorded in modernity was Jeanne Louise Calment, she died
in the age of 122 years and 164 days
[1]
.

There are rumors that the oldest tortoise called Adwaita (Aldabra giant
tortoise) died in the age of about 250 years
[2]
or that it was 188-year-old radiated tortoise named Tui Malila
[3]
, or that the highest verified age of 177 years had Galapagos giant
tortoise Harriet
[4]
. The oldest currently living turtle is considered to be Jonathan
(Seychelles giant tortoise), estimated to be over 180 years old these days
[5]
. Although all aforementioned numbers are estimations, it seems these
turtles were older than human supercentenarians.

All previously mentioned species are terrestrial tortoises, a group with
longest lifespans among turtles. The most famous of them, well-researched
Galapagos giant tortoise, was observed by Charles Darwin when he was
forming his well-known theory of evolution by natural selection
[6]
. There is only one freshwater turtle known to be able to outlive human, it
is the common snapping turtle estimated to live up to more than hundred
years
[7]
. While being considerably less researched, recorded maximal lifespan of
sea turtles is usually shorter, not exceeding 80 years, however, it is
believed that the green sea turtle can live up to 100 years.
[8]

It is a difficult question to answer why these reptiles can outlive us
because even to determine the actual age of animals with a long lifespan is
complicated – partially due to the fact that it takes such a long time to
study. Furthermore, many turtles are endangered species
[9]
so there may not be as many organisms to hand as needed for proper
statistics. Nonetheless, we can still claim that turtles are among the most
long-living vertebrates on earth
[10]
. Why?

Firstly, turtles, like all reptiles, benefit from being ectothermic
organisms. They do not maintain body temperature and thus save a lot of
energy. But that also means they are less flexible: it is crucial for their
lifespan to be in natural temperature environment of daily cycles with
night-time temperature drop
[11]
. If they do not live under these conditions in captivity, metabolic
pathways change and turtles die much sooner.
[12]

Turtles are well-adapted in other ways: their famous shell – the carapace
–is good protection against natural predators. Most of hatchling turtles
with a soft shell do not survive the first year
[13]
. A research of natural populations of freshwater turtles showed that only
one per cent of them can celebrate the twentieth birthdays, but once the
adulthood is reached, mortality rate drops and remains constant throughout
the rest of life
[14]
.

Some turtles can survive under extreme environmental conditions, such as
freezing
[15]
or lack of oxygen for months
[16]
. They can even undergo hibernation and anaerobic metabolism and therefore
deal with hypoxia and anoxia, it was also proposed that the same genes can
play a role in longevity itself
[17]
and also in oxidative stress resistance
[18]
that further promotes longer life
[19]
.

Turtle’s bones and shell are used as lactate buffer lowering metabolic
acidosis caused by anaerobic glycolysis during the period of lack of oxygen
[20]
;
[21]
Their organism is protected by strong innate immunity compensating slow
acquired immune reactions
[22]
.

Because turtles have very slow metabolism as well as growth, their bodies
do not need to deal with excessive metabolic heat and byproducts as mammals
[23]
. Their natural diet is very simple but also necessary for their longevity.
[24]

According to the evolutionary theories, staying alive is less important
after menopause. Galapagos giant tortoises achieve sexual maturity late
(around the age of up to forty years in the wild, and between twenty and
twenty-five years of life in captivity
[25]
), then staying fertile until death
[26]
.

The Hayflick limit is said to determine how many times a cell can divide
[27]
. The Hayflick limit of Galapagos giant tortoise was said to be about 110
divisions
[28]
, approximately twice as many as 50 of human cells
[29]
. Studies in this context have highlighted the importance of telomeres, the
protective end sequences of chromosomes, that get shorter with each cell
division
[30]
, can play at least a partially role in life expectancy. It was observed
that telomeres in European freshwater turtle’s cells are of the same length
in both embryo and adult organism
[31]
.

Thus, it was believed that turtles are negligibly senescent organisms
[32]
. In other words, the cells do not age and no age-related diseases appear,
which is very different cell behavior than in human bodies
[33]
and probably the key to any natural longevity. However, evidence now
suggests that turtles may not be really negligibly senescent because of
observations of survival and reproductive senescence in late age in the
painted turtle population
[34]

As we can see, turtles have some advantages in the lifespan field. Some of
these might inspire researchers to increase lifespans in humans.

by admin @ Alivebynature – Evidence Based Reviews

Sat Jan 20 06:51:06 PST 2018

Studies have shown that the food additive monosodium glutamate (MSG) may reduce appetite. However, this has only been examined in normal-weight adults, and the results have been inconsistent. For this reason, a group of researchers decided to research MSG consumption in overweight and obese women. Here is a detailed summary of their findings, recently published in the British […]

by @ Archive - Articles

Wed Jun 12 17:36:16 PDT 2013

What is LongeCity?
LongeCity is a registered, members-based non-profit organisation. More info here.

What THEMES of science projects does LongeCity support?
We support research into ageing and the extension of human lifespan. This means we support many types of medical research and research into basic biology, but there should be an angle that will allow people to live longer, healthier lives.

What TYPES of science projects does LongeCity support?
We support laboratory research, clinical research, bioinformatics and theoretical research in the ‘hard sciences’. We do not normally support social science research.
We do support some events, mentorship and travel to scientific conferences, but not under the ‘research budget’.

Where can the research take place?
Anywhere in the world. Laboratory research should normally be conducted in an established lab.

What does LongeCity expect in return?
Scientific integrity. Normally a written report. Interim updates for longer projects. Acknowledgement of the funding received. We may approach previous grantholders to be available as peer reviewers for future research applications.

What grant schemes are available?

a) Small GrantsFunding: up to $500Who can apply: any LongeCity Member, it helps if you have a sponsor/supervisor with some track recordType: typical cases are support for summer projects, internships, workshops, review paper writing, selected consumables Next deadline: none, applications are welcome until the annual budget is exhaustedDetails: http://www.longecity...s/action/grants

b) Matching FundraiserFunding: up to $20.000 (in total- matching fundraiser)Who can apply: ScientistsType: For selected projects, LongeCity will issue a call for donations and for every dollar received LongeCity will match (or better) the donation. The entire money goes to support the research project. Next deadline: July 1st 2013Details: http://www.longecity...ts/research2013

by @ ImmInst Active Topics

Sun Feb 11 17:35:26 PST 2018

Hey everyone,

Thank you in advance for taking the time to read and respond to my post. I’m a 23 year old (otherwise healthy) male who was diagnosed with lyme disease about two months ago. After undergoing an intense supplement/herbal/energetical therapy cleanse and detox, my docotor confirmed that the lyme had left my body. However, I am still experiencing all of my original symptoms, including random shaking, a neck tremor, intense brain fog, a really infammed gut/liver/kidneys, etc. I’m struggling to determine my next course of action — has anyone reading his post dealt with lyme? — have you tried dietary changes to help heal your system? I’m also curious if bpc 157 would be a good option for me? I already eat a fairly well balanced diet that is exclusively organic/non gmo, as well as taking about 15 relevant supplents a day (including probiotics). I guess, in general, I’m seeking any lyme, dietary, or other advice that you might have for me.

by medium bad @ Alivebynature – Evidence Based Reviews

Thu Jan 18 09:37:02 PST 2018

Aging has always been considered an inevitable process. But the discovery that the aging process itself could be ‘hacked’ has led to the concept of ‘health span’ as opposed to merely ‘lifespan’. A long life is not necessarily marred by disability and death and specific dietary interventions in particular may promote healthy long life. However, […]

by @ LongeCity - Articles

Wed Jul 18 18:44:43 PDT 2012

A) Background

LongeCity's origins lie with a personal website: On his private page where he chronicled his engagement with life extension, Bruce Klein also maintained a private bulleting board 'home for immortals'. Soon, visitors reached a critical mass.

And then it happened: Rather than staying at that level, we transcended it together. Bruce agreed to give up his control for something greater: the 'Immortality Institute' was founded as a members-based organisation.

This 'big tent' approach stood the test of time: Protagonists came and went, the original founders passed on the torch. The organisation endured, because it was no longer any individuals private agenda, it became an idea, a mission, and a community. We have left the days of the founding behind. We even changed our name, but, as an acknowledgement to this first, bold step into a unique community, LongeCity still refers to its internal Members section as the 'Immortality Institute' and remains open to Members from across the globe.

Also, until this day, our history shapes how we look at working with others: we celebrate the fantastic potential that lies in each person's own initiative and seek to empower individuals to pursue exactly those projects they feel passionate about, but we also try to link, to integrate, to join together and to collaborate in a broader context for maximum effect.

B) Private Individuals and their efforts/websites

There are many of personal websites around of the type Bruce started with. Some are just one person's way of discovering a new field, others grow into great resources or global benefit.
The great thing about them is the freedom they give you as the author to manage them largely as you please. Downsides exist: personal websites often have limited circulation beyond a particular social sphere or topic, missing chances for cross-pollination. A lot of energy is spent on re-inventing the wheel many times over, while it could be more productively channelled into improving what is already there. Mainly, they are fickle things, and anyone with internet experience learns not to trust them remaining as they often grind to a halt or disappear as the sole author/owner gets engaged in other priorities.

So on balance, LongeCity aims to make it easy for people to contribute directly to a larger pool. Members can have their own webspace or blogs or fora or linklists etc. without needing to home brew. If they want control, they can have as much as possible as long as it doesn't clash with others. (1)

On the other hand, some people only tap their full potential if they feel a project is fully and entirely their own.
IF that aspect is important to you, then please, by all means, do your own thing! We would much rather let a thousand flowers bloom than no growth at all. For maximum benefit, maybe you could still cross-reference to LongeCity? (2)

C) Other initiatives and Organisations

Now, this is a slightly more complicated topic.(3)

LongeCity understands itself as part of a movement. As usual in any movement, there are different preferences, protagonists, perspectives, powers and priorities. On the one hand, there is a real opportunity cost associated with not combining forces. It is sometimes very difficult to wish people good luck in setting up their own initiatives when, very clearly, their creative and financial resources could be much more effectively leveraged by using existing links and mechanisms.

On the other hand, different approaches and competition are absolutely essential to ensure that as many paths for success as possible are being pursued. LongeCity does not exist for its own sake. If it was not clear that we can make a unique contribution to the greater cause, we would close down and direct everyone to other initiatives. We need to be clear about what contribution we are making, when others are doing a better job and also when we are duplicating or being duplicated and why.

To all similar initiatives out there: If it looks like we are doing something very similar, please lets discuss if there are ways to generate greater synergies. This may simply mean that we stay in touch, it could mean collaboration on specific projects or it might go as far that LongeCity stops doing something and leaves it to you. OR you might decide to do what you are doing as part of LongeCity.

Two things in particular, we would much prefer to collaborate on:
1) if you are doing anything that involves a forum, we would be thrilled if you could do that at LongeCity. Over the years we have seen so many forums come and go, that we really think it a great shame to reinvent the wheel time and again. We'd gladly give you all the support and 'moderation' powers to run your own forum section at LongeCity, and a suite of powerful IT tools together with a great deal of experience as well.

2) if you are blogging or writing regular articles on life extension. Again, it is a great shame to see so many fantastic contributions swept away in the winds of time, whereas they could have been archived at LongeCity. We can easily supply you with all the tools and support, in fact we might even be able to pay you a little bit of money for your efforts - and the copyright still stays with you!

In summary, we have a mission, but not a specific 'line'. Instead we want to be a 'city'- a place where people come together. A place where different 'homes' exist fruitfully together, an umbrella group and a forum for exchange.
We would like to be a 'one-stop' info point for life extension on the web, from which people can move on to pick exactly those aspects or initiatives -at LongeCity or elsewhere- that they like. Any fellow initiatives out there, please get in touch to help make that vision a reality from which everyone benefits.

D) Advertisers at LongeCity

This is a slightly different topic. Anyone who visits LongeCity will not fail to notice that it attracts the attention of people who do not care much about our mission. Some come to debate, many to learn about nutrition (but not with an ultimate interest in life extension), some try to make money. To be quite frank, part of LongeCity's particular approach is to try to extract funds from these dynamics in order to re-allocate them towards the common mission. In this context, we sometimes partner with advertisers. Now, we do in fact discuss each advertiser internally and have rejected quite a few as not something we would affiliate with. However, at the end of the day the imperative is to raise money for a cause that we consider of life-saving importance. In that context we do not necessarily choose advertisers based on their own, (or their products) life-extension credentials. LongeCity does not endorse any advertisers beyond the fact that they have made a donation to the community in exchange for exposure. Advertisers never influence our policy, ever. Advertisers get banners (please click on them) -- thats it.
Having said that, advertisers featured at LongeCity very often have a real commitment to the cause- they would not have found us otherwise. When we say something nice about an advertiser, then that is NOT something they paid for but a genuine observation regarding their conduct and contribution to the cause.

E) Members representing LongeCity?

Membership of LongeCity is a strange thing: On the one hand, its a strictly in-or-out affair. On the other, Membership is just one way (and perhaps not a good one) to differentiate the 'talkers' from the 'doers'. If you are clearly a 'doer' we would probably consider you a Member of the life extension community whether you have joined the Immortality Institute or not. One way of simulating that is to give people 'points' for activities in connection with LongeCity. If you get enough points, Membership is free. Anyone who wants to join LongeCity but can't afford the (very modest) Membership donation, please get in touch, we have never denied membership to a committed peer based on inability to pay.
LongeCity is an open place. Membership as such does not entail 'vetting'.(4)

We hope that our Members conduct themselves in an exemplary manner that reflects well on the broader community at all times. But clearly, this is not always on the cards, not least because we are deliberately opening our doors to a diverse range of backgrounds and perspectives. Thus, whether someone is a Member does not mean that this person is in any way representative of our Membership or can speak on behalf of the organisation.

What about leadership? The case is not too different. Really, the only requirement to move into a leadership position at LongeCity is some tangible commitment. We don't vet people apart from a very basic appointment review and a requirement to sign the leadership agreement. Directors and certain key officers are asked for ID, but that's about it. Now, leaders *are* expected to behave in certain ways when representing LongeCity. Clearly, they owe as much to the Membership and community. But when not wearing the LongeCity hat, leaders are free to express their views and pursue their activities as they please and without any review by LongeCity. Some leaders may have gone on to do some strange things in their lives – LongeCity does not pry into a persons private affairs, successes or failures, ventures or missteps as long as it does not affect or organisation, community and mission.
If there is uncertainty whether a LongeCity leader is doing something in an official capacity, the fault is with us for allowing this ambiguity to prevail- please let us know and we'll make sure to clarify the situation.

F) CONCLUSION

The above are observations that I make from the Chair... but with the proviso that this perspective and policy might well change as time moves on – as you have seen from our history LongeCity is certainly able to evolve!
I hope the above is useful as a reference point regarding how LongeCity relates to 'others'. I also hope it has become clear that we really don't see a lot of 'others'. Anyone who shares our mission is 'one of us'. People interested in life extension are often individualists -- and any talk of a 'community' will need to take this into account. But mindful of this fact, as gently and effectively as possible, LongeCity aspires to provide a hospitable 'home' for a community, for diverse communitIES and lone travellers alike.

Footnotes:

(1) A good example of such a compromise are forum threads: A new discussion is initiated by a 'threadstarter'. A certain amount of responsibility comes with selecting a good topic, framing it well, giving it a good exposition. It can be frustrating if people spoil 'your' thread with inappropriate remarks. On your own website, you could just remove comments at will. On LongeCity, Members can ask to become Moderators of their own threads. It should be made clear in the first post if that option is used, so that other contributors are aware of this.

(2) For example, did you know that you can maintain a blog externally, AND a 'mirror' blog at LongeCity? Every post you make in your own blog can be automatically imported into your LongeCity blog. Ask if you need help setting this up.

(4) There are some conditions of membership --they are listed in our bylaws, and I shan't go into them here, but suffice it to say that it is not very difficult to join. Very few Members have ever been expelled and where that happened it was based on activities that were directly in connection with activities on the site. While Members might sometimes be rebuked or even banned from posting on our public forums, even that does not entail automatic removal of Membership.

by greg @ Canadian CattlemenCanadian Cattlemen

Thu Feb 08 10:58:18 PST 2018

Minerals are an essential part of a nutritionally balanced diet for beef cows. Unfortunately they are also a part of the diet that is overlooked due to the small inclusion rate. Those small inclusions are necessary to keep a cow running efficiently, making her capable of producing healthy, lively calves. The economics Minerals, such as […] Read more

by @ Articles

The oldest human recorded in modernity was Jeanne Louise Calment, she died
in the age of 122 years and 164 days
[1]
.

There are rumors that the oldest tortoise called Adwaita (Aldabra giant
tortoise) died in the age of about 250 years
[2]
or that it was 188-year-old radiated tortoise named Tui Malila
[3]
, or that the highest verified age of 177 years had Galapagos giant
tortoise Harriet
[4]
. The oldest currently living turtle is considered to be Jonathan
(Seychelles giant tortoise), estimated to be over 180 years old these days
[5]
. Although all aforementioned numbers are estimations, it seems these
turtles were older than human supercentenarians.

All previously mentioned species are terrestrial tortoises, a group with
longest lifespans among turtles. The most famous of them, well-researched
Galapagos giant tortoise, was observed by Charles Darwin when he was
forming his well-known theory of evolution by natural selection
[6]
. There is only one freshwater turtle known to be able to outlive human, it
is the common snapping turtle estimated to live up to more than hundred
years
[7]
. While being considerably less researched, recorded maximal lifespan of
sea turtles is usually shorter, not exceeding 80 years, however, it is
believed that the green sea turtle can live up to 100 years.
[8]

It is a difficult question to answer why these reptiles can outlive us
because even to determine the actual age of animals with a long lifespan is
complicated – partially due to the fact that it takes such a long time to
study. Furthermore, many turtles are endangered species
[9]
so there may not be as many organisms to hand as needed for proper
statistics. Nonetheless, we can still claim that turtles are among the most
long-living vertebrates on earth
[10]
. Why?

Firstly, turtles, like all reptiles, benefit from being ectothermic
organisms. They do not maintain body temperature and thus save a lot of
energy. But that also means they are less flexible: it is crucial for their
lifespan to be in natural temperature environment of daily cycles with
night-time temperature drop
[11]
. If they do not live under these conditions in captivity, metabolic
pathways change and turtles die much sooner.
[12]

Turtles are well-adapted in other ways: their famous shell – the carapace
–is good protection against natural predators. Most of hatchling turtles
with a soft shell do not survive the first year
[13]
. A research of natural populations of freshwater turtles showed that only
one per cent of them can celebrate the twentieth birthdays, but once the
adulthood is reached, mortality rate drops and remains constant throughout
the rest of life
[14]
.

Some turtles can survive under extreme environmental conditions, such as
freezing
[15]
or lack of oxygen for months
[16]
. They can even undergo hibernation and anaerobic metabolism and therefore
deal with hypoxia and anoxia, it was also proposed that the same genes can
play a role in longevity itself
[17]
and also in oxidative stress resistance
[18]
that further promotes longer life
[19]
.

Turtle’s bones and shell are used as lactate buffer lowering metabolic
acidosis caused by anaerobic glycolysis during the period of lack of oxygen
[20]
;
[21]
Their organism is protected by strong innate immunity compensating slow
acquired immune reactions
[22]
.

Because turtles have very slow metabolism as well as growth, their bodies
do not need to deal with excessive metabolic heat and byproducts as mammals
[23]
. Their natural diet is very simple but also necessary for their longevity.
[24]

According to the evolutionary theories, staying alive is less important
after menopause. Galapagos giant tortoises achieve sexual maturity late
(around the age of up to forty years in the wild, and between twenty and
twenty-five years of life in captivity
[25]
), then staying fertile until death
[26]
.

The Hayflick limit is said to determine how many times a cell can divide
[27]
. The Hayflick limit of Galapagos giant tortoise was said to be about 110
divisions
[28]
, approximately twice as many as 50 of human cells
[29]
. Studies in this context have highlighted the importance of telomeres, the
protective end sequences of chromosomes, that get shorter with each cell
division
[30]
, can play at least a partially role in life expectancy. It was observed
that telomeres in European freshwater turtle’s cells are of the same length
in both embryo and adult organism
[31]
.

Thus, it was believed that turtles are negligibly senescent organisms
[32]
. In other words, the cells do not age and no age-related diseases appear,
which is very different cell behavior than in human bodies
[33]
and probably the key to any natural longevity. However, evidence now
suggests that turtles may not be really negligibly senescent because of
observations of survival and reproductive senescence in late age in the
painted turtle population
[34]

As we can see, turtles have some advantages in the lifespan field. Some of
these might inspire researchers to increase lifespans in humans.